Ferroptosis Cancer Research Results

Ferroptosis, Ferroptosis: Click to Expand ⟱

Source:

Type: type of cell death

Type of programmed cell death dependent on iron.
Ferroptosis is a form of regulated cell death characterized by the accumulation of lipid peroxides to lethal levels. It is distinct from other forms of cell death, such as apoptosis, necrosis, and autophagy. The process of ferroptosis is heavily dependent on iron metabolism and reactive oxygen species (ROS).
The accumulation of lipid peroxides is a hallmark of ferroptosis. This can occur when the antioxidant defenses, such as glutathione and selenoproteins, are overwhelmed or inhibited. Many cancer cells upregulate GPX4 to evade ferroptosis, making it a potential target for therapy. It has been described that GPX4, xCT and ACSL-4 are the main targets in the regulation of ferroptosis.

Scientific Papers found: Click to Expand⟱

5263-

3BP,

CET,

3-Bromopyruvate overcomes cetuximab resistance in human colorectal cancer cells by inducing autophagy-dependent ferroptosis

in-vitro,

CRC,

DLD1

NA,

HCT116

eff↑, Our results demonstrated that the co-treatment of 3-BP and cetuximab synergistically induced an antiproliferative effect in both CRC cell lines
Ferroptosis↓, co-treatment induced ferroptosis, autophagy, and apoptosis.
TumAuto↑,
Apoptosis↑,
FOXO3↑, co-treatment inhibited FOXO3a phosphorylation and degradation and activated the FOXO3a/AMPKα/pBeclin1 and FOXO3a/PUMA pathways, leading to the promotion of ferroptosis, autophagy, and apoptosis in DLD-1
AMPKα↑,
p‑Beclin-1↑,
HK2↓, 3-Bromopyruvate (3-BP), also known as hexokinase II inhibitor II, has shown promise as an anticancer agent against various types of cancer
ATP↓, 3-BP exerts its anticancer effects by manipulating cell energy metabolism and regulating oxidative stress, as evidenced by the accumulation of reactive oxygen species (ROS) [13,14,15,16].
ROS↑,
Dose↝, Eight days postinoculation, xenografted mice were randomly divided into four groups and intraperitoneally injected with PBS, 3-BP, cetuximab, or a combination of 3-BP and cetuximab every four days for five injections.
TumVol↓, 3-BP alone or co-treatment with 3-BP and cetuximab significantly reduced the tumor volume and tumor weight on Day 28, but co-treatment showed a greater reduction than 3-BP alone
TumW↓,
xCT/SLC7A11↑, The protein level of SLC7A11 was significantly upregulated in all three cell lines following co-treatment (Fig. 2B).
GSH↓, co-treatment with 3-BP and cetuximab led to glutathione (GSH) depletion (Fig. 2D), reactive oxygen species (ROS) production
eff↓, Knockdown of either ATG5 or Beclin1 attenuated the cell death and MDA production induced by co-treatment
MDA↑,

4991-

ART/DHA,

doxoR,

Dihydroartemisinin alleviates doxorubicin-induced cardiotoxicity and ferroptosis by activating Nrf2 and regulating autophagy

in-vivo,

Nor,

H9c2

gavage for 4 weeks in mice.

*cardioP↑, In vivo, DHA markedly relieved Dox-induced cardiac dysfunction, attenuated oxidative stress, alleviated cardiomyocyte ferroptosis, activated Nrf2, promoted autophagy, and improved the function of lysosomes.
*ROS↓,
*Ferroptosis↓,
*NRF2↑,
Keap1↓, DHA significantly alleviates Dox-induced ferroptosis through the clearance of autophagosomes, including the selective degradation of keap1 and the recovery of lysosomes.

2625-

Ba,

LT,

Baicalein and luteolin inhibit ischemia/reperfusion-induced ferroptosis in rat cardiomyocyte

in-vivo,

Stroke,

rat

*lipid-P↓, Baicalein and luteolin prevented the Fe-SP-induced lipid peroxidation in rat neonatal cardiomyocytes.
*ACSL4∅, Baicalein and luteolin can reduce the protein levels of ACSL4 and Nrf2, and enhance the protein levels of GPX4 in ischemia/reperfusion-treated rat hearts.
*NRF2∅, Our results suggest that BAI and Lut prevented the I/R-induced increased of ACSL4, NRF2, and HO-1 protein
*GPx4∅, BAI and Lut prevented the I/R-induced increased of ACSL4, NRF2, and HO-1 protein, and the I/R-decreased GPX4 protein levels
*Ferroptosis↓, BAI was found to suppress ferroptosis in cancer cells via reducing reactive oxygen species (ROS) generation.
*ROS↓,
*MDA↓, Moreover, both BAI and Lut decreased ROS and malondialdehyde (MDA) generation and the protein levels of ferroptosis markers, and restored Glutathione peroxidase 4 (GPX4) protein levels in cardiomyocytes reduced by ferroptosis inducers
*eff↑, BAI and Lut reduced the I/R-induced myocardium infarction
*HO-1∅, Our results suggest that BAI and Lut prevented the I/R-induced increased of ACSL4, NRF2, and HO-1 protein

2628-

Ba,

Cisplatin,

Baicalein alleviates cisplatin-induced acute kidney injury by inhibiting ALOX12-dependent ferroptosis

in-vitro,

Nor,

HK-2

*RenoP↑, Baicalein alleviated cisplatin- and folic acid-induced renal dysfunction and pathological damage and improved cisplatin-induced HK2 cell injury
*12LOX↓, Mechanistically, baicalein reduced the expression of 12-lipoxygenase (ALOX12), which inhibits phospholipid peroxidation and ferroptosis in AKI
*Ferroptosis↓,

2626-

Ba,

Molecular targets and therapeutic potential of baicalein: a review

Review,

Var,

Review,

AD,

Review,

Stroke,

AntiCan↓, anticancer, antidiabetic, antimicrobial, antiaging, neuroprotective, cardioprotective, respiratory protective, gastroprotective, hepatic protective, and renal protective effects
*neuroP↑,
*cardioP↑, Cardioprotective action of baicalein
*hepatoP↑,
*RenoP↑, baicalein’s capacity to lessen cisplatin-induced nephrotoxicity is probably due, at least in part, to the attenuation of renal oxidative and/or nitrative stress
TumCCA↑, Baicalein induces G1/S arrest in lung squamous carcinoma (CH27) cells by downregulating CDK4 and cyclin D1, as well as upregulating cyclin E
CDK4↓,
cycD1/CCND1↓,
cycE/CCNE↑,
BAX↑, SGC-7901 cells showed that when baicalein was administered, Bcl-2 was downregulated and Bax was increased
Bcl-2↓,
VEGF↓, Baicalein inhibits the synthesis of vascular endothelial growth factor (VEGF), HIF-1, c-Myc, and nuclear factor kappa B (NF-κB) in the G1 and S phases of ovarian cancer cell
Hif1a↓,
cMyc↓,
NF-kB↓,
ROS↑, Baicalein produced intracellular reactive oxygen species (ROS) and activated BNIP3 to slow down the development and hasten the apoptosis of MG-63,OS cell
BNIP3↑,
*neuroP↑, Baicalein exhibits neuroprotective qualities against amyloid (AN) functions by preventing AN from aggregating in PC12 neuronal cells to cause A𝛽-induced cytotoxicity
*cognitive↑, baicalein encourages non-amyloidogenic processing of APP, which lowers the generation of A𝛽 and enhances cognitive function
*NO↓, baicalein effectively reduced NO generation and iNOS gene expression
*iNOS↓,
*COX2/PTGS2↓, Baicalein therapy significantly decreased the expression of COX-2 and iNOS, as well as PGE2 and NF-κB, indicating a protective effect against cerebral I/R injury.
*PGE2↓,
*NRF2↑, Baicalein therapy markedly elevated nuclear Nrf2 expression and AMPK phosphorylation in the ischemic cerebral cortex
*p‑AMPK↑,
*Ferroptosis↓, Baicalein suppressed ferroptosis associated with 12/15-LOX, hence lessening the severity of post-traumatic epileptic episodes generated by FeCl3
*lipid-P↓, HT22 cells were damaged by ferroptosis, which is mitigated by baicalein may be due to its lipid peroxidation inhibitor
*ALAT↓, Baicalin lowers the raised levels of hepatic markers alanine transaminase (ALT), aspartate aminotransferase (AST)
*AST↓,
*Fas↓, Baicalin has also been shown to suppress apoptosis, decrease FAS protein expression, block the caspase-8 pathway, and decrease Bax protein production
*BAX↓,
*Apoptosis↓,

2701-

BBR,

Berberine Inhibits KLF4 Promoter Methylation and Ferroptosis to Ameliorate Diabetic Nephropathy in Mice

in-vivo,

Diabetic,

MICE

*Inflam↓, Berberine has various biological activities, including anti-inflammation, antioxidative stress, and antiferroptosis
*antiOx↑,
*Ferroptosis↓,
*RenoP↑, Berberine rescued kidney function and renal structure and prevented renal fibrosis in diabetic nephropathy mice.
*DNMT1↓, Berberine suppressed the expression of DNMT1 and DNMT2 and upregulated KLF4 expression by preventing KLF4 promoter methylation.
*DNMTs↓,
*KLF4↑,

3679-

BBR,

Berberine alleviates Alzheimer's disease by activating autophagy and inhibiting ferroptosis through the JNK-p38MAPK signaling pathway

in-vivo,

AD,

5xFAD mice

*Beclin-1↑, autophagy-related markers Beclin1 and LC3B were upregulated and P62 was downregulated after BBR treatment.
*LC3B↑,
*p62↓,
*ROS↓, ROS and lipid peroxide MDA decreased significantly after BBR treatment.
*lipid-P↓,
*MDA↓,
*Ferroptosis↓, expression levels of ferroptosis-related genes TFR1, ASCL4, DMT1, and IREB2 were decreased, while the expression levels of FTH1 and SLC7A11 increased after BBR treatment.
*TfR1/CD71↓,
*FTH1↑,
*memory↑, BBR treatment enhanced spatial memory impairment in 5xFAD mice.
*JNK↓, inhibited ferroptosis by inhibiting the JNK-P38MAPK signaling pathway.
*p38↓,
*Aβ↓, further reducing Aβ plaque deposition, inhibiting inflammatory response,
*Inflam↓,

5925-

CAR,

Neuroprotective effects of carvacrol against Alzheimer’s disease and other neurodegenerative diseases: A review

Review,

AD,

Review,

Park,

Review,

Stroke,

*Inflam↓, anti-inflammatory, antioxidant, and AChEI properties
*antiOx↑,
*AChE↓,
*BBB↑, Carvacrol is able to cross the blood brain barrier easily, notably improving its therapeutic efficacy in neurodegenerative disorders
*cardioP↑, prevention of many chronic diseases, such as cancer as well as infectious, cardiovascular and neurodegenerative diseases
*neuroP↑, Extensive researches have revealed carvacrol neuroprotective properties
*memory↑, memory-enhancing activities
*TAC↑, Carvacrol has antioxidant activity and was shown to act as a dietary phyto-additive to boost animal antioxidant status (sharifi-Rad et al., 2018
*ROS↓, carvacrol could protect neuronal injuries against Aluminum-induced oxidative stress leading to lipid peroxidation
*lipid-P↓,
*MDA↓, carvacrol has been indicated to reduce malondialdehyde (MDA) and neuronal cell necrosis, and increase superoxide dismutase (SOD) and catalase (CAT) activity levels in the hippocampus (
*SOD↑,
*Catalase↑,
*NRF2↑, carvacrol activated nuclear factor-erythroid 2-related factor 2 (Nrf2) as an endogenous antioxidant
*cognitive↑, Carvacrol administration (25, 50, and 100 mg/kg) during 21 days attenuated memory impairments and enhanced cognition compared to the control group.
*IL1β↓, Carvacrol administration diminished the expression of interleukin-1β (IL-1β), cyclooxygenase-2 (COX-2), and tumor necrosis factor-α (TNF-α).
*COX2/PTGS2↓,
*TNF-α↓,
*TLR4↓, carvacrol could significantly decrease Toll-like receptor 4 (TLR4) and increase brain-derived neurotrophic factor (BDNF) expression.
*BDNF↑,
*PKCδ↑, carvacrol and thymol might have protective ability on cognitive function in AD by activation of PKC pathway
*5LO↓, Carvacrol inhibited AChE and lipoxygenase activity that supports its anti-inflammation and anti-Alzheimer effects
*TRPM7↓, Reduced caspase-3 levels, and TRPM7 channels inhibitor
*GSH↑, Antioxidant activity, Increased glutathione
*other↑, revealed a remarkable neuroprotective action of carvacrol in cerebral ischemia in animal models
*Ferroptosis↓, via ferroptosis inhibition by elevating GPx4 expression
*GPx4↑,

6013-

CGA,

Advances in Pharmacological Properties, Molecular Mechanisms, and Bioavailability Strategies of Chlorogenic Acid in Cardiovascular Diseases Therapy

Review,

CardioV,

*BioAv↝, As a dietary component, CGA exhibits moderate oral bioavailability [9], and its molecular structure remains largely intact during oral digestion
*BioAv↝, The composition of gut microbiota plays a critical role in CGA’s metabolism and absorption, producing 11 key metabolites, with the most primary products dihydrocaffeic acid, dihydroferulic acid, and 3-(3-hydroxyphenyl) propionic acid [
*BP↓, eported that CGA lowers blood pressure by relaxing vascular smooth muscle and improving endothelial function
*ROS↓, inhibiting the sources of reactive oxygen species (ROS), such as NADPH oxidase,
*NADPH↓,
*AntiAg↑, he downregulation of thromboxane A2 plays a crucial role in CGA-mediated inhibition of platelet aggregation
*TXA2↓,
*antiOx↑, cCGA exhibited the strongest antioxidant effect, which may be related to improved mitochondrial function [
*cardioP↑, CGA exerts significant cardioprotective effects by modulating multiple signaling pathways.
*Inflam↓, reduce infarct size in MI induced by left anterior descending artery (LAD) ligation in rats. It achieves this by suppressing inflammation and enhancing the activity of antioxidant enzymes, such as SOD and CAT, thereby improving cardiac function
*SOD↑,
*Catalase↑,
*Ferroptosis↓, CGA’s ability to alleviate ferroptosis
*NF-kB↓, inhibiting the NF-κB and JNK signaling pathways, highlighting its cardioprotective potential in a TAC mouse model
*JNK↓,
*NRF2↑, CGA reduces oxidative stress and ROS-induced damage by upregulating the Nrf2/HO-1 pathway, thereby mitigating doxorubicin-induced cardiotoxicity and improving cardiac tissue integrity
*HO-1↑,
*toxicity↓, which are widely used in traditional Chinese medicine [60,61], it is generally considered safe.
*BioAv↓, CGA struggles to cross lipophilic membranes, resulting in poor absorption and bioavailability [69]. Simply increasing the oral dose is not an advisable solution, as it carries significant risks.
*BioAv↑, in vitro study reported that the covalent bonding between CGA and soluble oat β-glucan significantly improved CGA’s structural stability and maximized its pharmacological potential
*BioAv↑, Studies have reported that CGA-loaded liposomes, prepared from cholesterol and phosphatidylcholine, showed a relative oral bioavailability of 129.38% compared to free CGA.
eff↑, bovine serum albumin (BSA)-decorated chlorogenic acid silver nanoparticles (AgNPs-CGA-BSA) exhibited significant antioxidant and anticancer effects both in vitro and in vivo.

6210-

CUR,

Potential Roles and Mechanisms of Curcumin and its Derivatives in the Regulation of Ferroptosis

Ferroptosis↑, curcumin is a ferroptosis inducer with excellent anticancer efficacy, although it also exhibits organ protective and reparative effects by acting as a ferroptosis inhibitor.
*Ferroptosis↓,
ROS↑, Accumulated intracellular iron is the trigger for ferroptosis as it can produce highly reactive free radicals via the Fenton reaction, which can lead to ferroptosis
Fenton↑,
*IronCh↑, ability of curcumin to chelate iron and regulate oxidation predicts that curcumin may have a role in regulating ferroptosis,
GPx4↓, Curcumin and its derivative EF24 repress GPX4 expression and increase MDA and ROS levels to exert a pro-ferroptosis effect in osteosarcoma cells
MDA↑,
GSH↓, reduction in GSH content and L-OOH levels was measured in curcumin-treated TNBC cells
*NRF2↑, protective effects against ferroptosis-induced damage to cells107. Through activation of the Nrf2/HO-1 pathway, curcumin can both restrict high glucose-induced neuronal (N2a) cell injury
*HO-1↑,

4990-

Dipy,

Characterization of dipyridamole as a novel ferroptosis inhibitor and its therapeutic potential in acute respiratory distress syndrome management

in-vivo,

Nor,

*Ferroptosis↓, These findings provide compelling evidence that DIPY inhibits ferroptosis in pulmonary epithelial and endothelial cells by modulating the SOD1/CREB1/HMOX1 signaling axis and suggest DIPY as a promising therapeutic strategy for ARDS treatment.
*HO-1↓, effectively mitigated ferroptosis and pulmonary damage in both mouse models and hAOs, primarily by downregulating heme oxygenase 1 (HMOX1).
SOD1↑, DIPY binds to and activates superoxide dismutase 1 (SOD1), which in turn inhibits the CREB1/HMOX1 pathway, thereby suppressing ferroptosis.

6983-

Form,

Formononetin enhances angiogenesis in diabetic wounds by inhibiting ferroptosis through suppression of mtROS-mediated xCT/GPX4 upregulation

vitro+vivo,

Nor,

HUVECs

mice

vitro+vivo,

Diabetic,

*BloodF↑, Formononetin (FMN), a phytoestrogen from Astragalus roots, is traditionally used to enhance blood function and microcirculation; however, its mechanism remains unclear.
*Ferroptosis↓, FMN effectively reduced ferroptosis markers in HG-treated HUVECs,
*eff↓, and Erastin treatment abolished this protective effect.
*mtDam↓, block ferroptosis through two mechanisms: restoration of mitochondrial integrity and reactivation of the xCT/GPX4 antioxidant system
*xCT/SLC7A11↑,
*GPx4↑,
*Wound Healing↑, When we tested FMN in diabetic mice, wound closure rates improved substantially, the expression of xCT and GPX4 was increased, and CD31 expression in wound vessels increased, which matched what we observed in vitro.
*CD31/PECAM-1↑,
*mt-ROS↓, mitigation of mitochondrial reactive oxygen species (mtROS) accumulation through xCT/GPX4 activation.

3761-

H2,

Therapeutic Inhalation of Hydrogen Gas for Alzheimer's Disease Patients and Subsequent Long-Term Follow-Up as a Disease-Modifying Treatment: An Open Label Pilot Study

Human,

AD,

inhaled 3% H2 gas for one hour twice daily for 6 months

*cognitive↑, the mean individual ADAS-cog change showed significant improvement after 6 months of H2 treatment (−4.1) vs. untreated patients (+2.6).
*BBB↑, H2 has the ability to cross the blood-brain barrier (BBB) by gaseous diffusion without a specific drug delivery system
*ROS↓, An oxidized form of porphyrin catalyzes the reaction of H2 with hydroxyl radicals, the most oxidative free radicals, to reduce the oxidative stress.
*NRF2↑, secondary anti-oxidative function, H2 activates NF-E2-related factor 2 (Nrf2) [9], which reduces oxidative stress through the expression of a variety of anti-oxidant enzymes
*Inflam↓, H2 relieves inflammation by decreasing pro-inflammatory cytokines [38].
*NFAT↓, resulting in suppressing the nuclear factor of activated T cell (NFAT) transcription pathway to down-regulate pro-inflammatory cytokines
*FAO↓, H2 inhibits the free radical chain reaction, resulting in a decrease in fatty acid peroxidation and its end-products such as 4-hydroxyl-nonenal (4-HNE),
*4-HNE↓,
*PGC-1α↑, In turn, the decrease in 4-HNE promotes the expression of PGC-1α, followed by increasing FGF21,
*Ferroptosis↓, H2 has an anti-cell-death function by inhibiting ferroptosis through a decrease in peroxide [36], and by down- and up-regulating pro- and anti-death factors, respectively

7562-

HYP,

doxoR,

Hyperoside Inhibits Doxorubicin-Induced Ferroptosis in Cardiomyocytes via the Nrf2/GPX4 Pathway

in-vivo,

Nor,

urine model of DOX-induced cardiotoxicity with Hyp co-treatment.

*ROS↓, Hyperoside (Hyp) exhibits notable protective effects by targeting oxidative stress, ferroptosis, and apoptosis.
*Ferroptosis↓,
*Apoptosis↓,
*cardioP↑, Hyp co-administration mitigated doxorubicin-induced cardiac impairment in mice, demonstrated by enhanced ejection fraction (EF) and fractional shortening (FS), diminished inflammatory cell infiltration and fibrotic changes
*MDA↓, Hyp reduced oxidative stress (lower MDA, higher SOD and GSH-Px activity), inhibited ferroptosis (decreased intracellular Fe2 + , MDA, 4-HNE, PTGS2, and ASCL4; increased GSH and Ferritin),
*SOD↑,
*GPx↑,
*i-Iron↓,
*4-HNE↓,
*GSH↑,
*Ferritin↑,
*ACSL4↓,
*NRF2↑, Mechanistically, Hyp activated the Nrf2/GPX4 axis: it promoted Nrf2 nuclear translocation, upregulated GPX4 expression as shown by molecular docking.
*GPx4↑,

7766-

ISL,

Isoliquiritigenin alleviates myocardial ischemia-reperfusion injury by regulating the Nrf2/HO-1/SLC7a11/GPX4 axis in mice

in-vivo,

Stroke,

mice

*ROS↓, ISL significantly attenuated H/R-triggered production of reactive oxygen species in NMCM, reduced the expression of malondialdehyde and the activity of lactate dehydrogenase, enhanced superoxide dismutase and catalase activity,
*MDA↓,
*LDH↑,
*SOD↑,
*Catalase↑,
*NRF2↑, and increased the expression of nuclear factor E2-related factor 2 (Nrf2) and its downstream heme oxygenase 1 (HO-1), thereby mitigating oxidative stress damage.
*i-Iron↓, ISL reduced intracellular free iron accumulation, up-regulated glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) expression, and inhibited lipid peroxidation accumulation, thereby alleviating ferroptosis.
*GPx4↑,
*xCT/SLC7A11↑,
*lipid-P↓,
*Ferroptosis↓,
*HO-1↑, ISL treatment increased the levels of HO-1, GPX4, and SLC7A11, inhibited the expression of ACSL4
*ACSL4↓,
*mtDam↓, alleviated mitochondrial damage, and ferroptosis, ultimately reducing myocardial infarction area and injury induced by I/R.
*Stroke↓,

7812-

ISQ,

Isoquercitrin promotes ferroptosis and oxidative stress in nasopharyngeal carcinoma via the AMPK/NF-κB pathway

vitro+vivo,

NPC,

CNE1

392.45

in-vitro,

NPC,

HNE1

411.38 μM

tumCV↓, CNE1 and HNE1 viability and proliferation were both markedly reduced with the increasing concentration of isoquercitrin.
TumCP↓,
ROS↑, ROS generation and lipid peroxidation were both enhanced with declined ferroptosis-related markers under isoquercitrin treatment.
lipid-P↑,
NF-kB↓, (NF-κB) pathway, the AMPK pathway, and the interleukin (IL)-1β expression were all markedly suppressed by isoquercitrin
MAPK↓,
IL1β↓,
TumCG↓, isoquercitrin restrained the tumor growth and enhanced lipid peroxidation and ferroptosis in vivo.
lipid-P↓,
Ferroptosis↓,
eff↓, Interestingly, both Fer-1 and ALA treatments distinctly offset isoquercitrin-induced effects in vitro and in vivo.

2956-

PL,

Piperlongumine rapidly induces the death of human pancreatic cancer cells mainly through the induction of ferroptosis

in-vitro,

PC,

ROS↑, Piperlongumine (PL) is a natural product with cytotoxic properties restricted to cancer cells by significantly increasing intracellular reactive oxygen species (ROS) levels.
Ferroptosis↓, at least in part, the induction of ferroptosis,. requires the accumulation of ROS in an iron-dependent manner
GSH↓, Since we actually found that PL markedly depleted GSH (Fig. 1H), these results suggest that PL may inhibit GPX activity.
GPx↓,
cl‑PARP∅, PL did not induce the expression of typical apoptotic markers, such as cleaved PARP and cleaved caspase-3
cl‑Casp3∅,
eff↑, PL (15 uM) plus CN-A resulted in a further increase in the population of ROS-positive cells
eff↑, SSZ enhances the PL-induced ferroptotic death of pancreatic cancer cells.

3023-

RosA,

Rosmarinic acid alleviates septic acute respiratory distress syndrome in mice by suppressing the bronchial epithelial RAS-mediated ferroptosis

in-vivo,

Sepsis,

*GPx4↑, RA notably inhibited the infiltration into the lungs of neutrophils and monocytes with increased amounts of GPX4 and ACE2 proteins, lung function improvement,
*Inflam↓, decreased inflammatory cytokines levels and ER stress in LPS-induced ARDS in mice.
*ER Stress↓,
*Ferroptosis↓, the anti-ferroptosis effect of RA in LPS-induced septic
*Sepsis↓,
*GRP78/BiP↓, Previously, we reported that RA markedly ameliorated septic-associated mortality and lung injury via inhibiting GRP78/IRE1α/JNK pathway-mediated ERS
*IRE1↓,
JNK↓,

3024-

RosA,

rmMANF prevents sepsis-associated lung injury via inhibiting endoplasmic reticulum stress-induced ferroptosis in mice

in-vivo,

Sepsis,

*Ferroptosis↓, rmMANF pretreatment inhibits ferroptosis by suppressing GRP78/PERK/ATF4 axis.
*GRP78/BiP↓,
*PERK↓,
*ATF4↓,
*Sepsis↓,
*GSH↑, LPS administration mice exhibited elevated MDA immunoactivity, total iron level, and declined GSH level, and SOD, CAT activities, while these effects of LPS were effectively against by rmMANF pretreatment
*SOD↑,
*Catalase↑,

3039-

RosA,

Rosmarinic acid liposomes suppress ferroptosis in ischemic brain via inhibition of TfR1 in BMECs

in-vivo,

Nor,

mice

in-vivo,

Stroke,

*Ferroptosis↓, RosA-LIP inhibited ferroptosis by ameliorating mitochondrial abnormalities, increasing GPX4 levels, and decreasing ACSL4/LPCAT3/Lox-dependent lipid peroxidation.
*GPx4↑,
*ACSL4↓,
*BBB↑, RosA-LIP effectively improved blood‒brain barrier (BBB) permeability, increased tight junctions (TJs) protein expression
*IronCh↑, reduced iron levels in ischemic tissue and brain microvascular endothelial cells (BMECs) by modulating FPN1 and TfR1 levels.
*TfR1/CD71↓, Furthermore, RosA-LIP suppressed TfR1 to attenuate ACSL4/LPCAT3/Lox-mediated ferroptosis in TfR1EC cKO mice subjected to dMCAO.
*neuroP↑, proposed neuroprotection of RosA-LIP during ischemic stroke.

3313-

SIL,

Silymarin attenuates post-weaning bisphenol A-induced renal injury by suppressing ferroptosis and amyloidosis through Kim-1/Nrf2/HO-1 signaling modulation in male Wistar rats

in-vivo,

NA,

50-100 mg/kg/day

Twenty-four male Wistar rats

*NRF2↑, silymarin activates the Nrf2/HO-1 pathway, thus providing cellular defense
*HO-1↑,
*creat↓, Silymarin diminished BPA-induced rise in serum urea, creatinine, BUN, and plasma kim-1 levels.
*BUN↓,
*RenoP↑, improved renal histoarchitecture in BPA-exposed rats.
*MDA↓, suppression of BPA-induced rise in renal iron, MDA, TNF-α, IL-1β, and cytochrome c levels, and myeloperoxidase and caspase 3 activities by silymarin therapy.
*TNF-α↓,
*IL1β↓,
*Cyt‑c↓,
*Casp3↓,
*GSTs↓, silymarin attenuated BPA-induced downregulation of Nrf2 and GSH levels, and HO-1, GPX4, SOD, catalase, GST, and GR activities.
*GSH↑,
*GPx4↑,
*SOD↑,
*GSR↓,
*Ferroptosis↓, silymarin mitigated post-weaning BPA-induced renal toxicity by suppressing ferroptosis and amyloidosis through Kim-1/Nrf2/HO-1 modulation.

2201-

SK,

Shikonin promotes ferroptosis in HaCaT cells through Nrf2 and alleviates imiquimod-induced psoriasis in mice

in-vitro,

PSA,

HaCaT

in-vivo,

NA,

mice

*eff↑, SHK treatment significantly improved imiquimod (IMQ)-induced psoriasis symptoms in mice
*IL6↓, attenuated the production of inflammatory cytokines, including interleukin (IL)-6, IL-17, and tumor necrosis factor-alpha (i.e., TNF-α)
*IL17↓,
*TNF-α↓,
*lipid-P↑, enhancing intracellular and mitochondrial ferrous and lipid peroxidation levels
*NRF2↓, by regulating expression of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), nuclear receptor coactivator 4 (NCOA4) and glutathione peroxidase 4 (GPX4)
*HO-1↝,
*NCOA4↝,
*GPx4↓, low dose SHK on LPS inhibited GPX4 and Nrf2 expression
*Ferroptosis↓, inhibited ferroptosis in psoriatic skin by reducing inflammation, ameliorating oxidative stress and iron accumulation.
*Inflam↓,
*ROS↓,
*Iron↓,

2195-

SK,

Shikonin induces ferroptosis in osteosarcomas through the mitochondrial ROS-regulated HIF-1α/HO-1 axis

in-vitro,

OS,

TumCP↓, At a low dose, Shikonin inhibits OS progression and has a excellent biosafety.
Ferroptosis↓, Shikonin induces ferroptosis in OS cel
Hif1a↑, Shikonin upregualtes HIF-1α/HO-1 axis to produce excess Fe2+ which leads to ROS accumulation on OS cell, followed by ferroptosis.
HO-1↑,
Iron↑,
ROS↑,
GSH/GSSG↓, while simultaneously reducing the GSH/GSSG ratio and GPX4 and SLC7A11 expression
GPx4↓,

4727-

SSE,

Selenium inhibits ferroptosis in ulcerative colitis through the induction of Nrf2/Gpx4

in-vivo,

Col,

experimental colitis in mice treated with dextran sulfate sodium (DSS)

*Ferroptosis↓, Selenium can relieve DSS-induced colitis and inhibit IECs ferroptosis by up-regulating the expression of Nrf2/Gpx4.
*NRF2↑,
*GPx4↑,
*eff↑, The in vivo results showed that selenium treatment could improve IECs colitis induced by DSS and inhibit ferroptosis.
*other↓, The serum selenium content of UC patients was lower than that of healthy subjects.
*antiOx↑, Selenium, an essential micronutrient of human, which has the functions of anti-oxidation, immune regulation, anti-inflammatory and anti-tumor
*Inflam↓,
AntiTum↑,

4732-

SSE,

Selenium inhibits ferroptosis and ameliorates autistic-like behaviors of BTBR mice by regulating the Nrf2/GPx4 pathway

in-vivo,

Autism,

BTBR mice

*Ferroptosis↓, Selenium inhibits ferroptosis and ameliorate abnormal behavior via the Nrf2/Gpx4 signaling pathway.
*NRF2↑, Treatment with Se increased levels of Nrf2 and GPX4.
*GPx4↑,
*other↝, Se exhibited a beneficial effect on autism-relevant behaviors and inhibited ferroptosis in the BTBR mouse model of ASD, possibly through modulation of the Nrf2/GPX4 signaling pathway.

4869-

Uro,

Urolithin A in Central Nervous System Disorders: Therapeutic Applications and Challenges

Review,

AD,

Review,

Park,

Review,

Stroke,

*MitoP↑, key biological effects of UA, including its promotion of mitophagy and mitochondrial homeostasis, as well as its anti-inflammatory, antioxidant, anti-senescence, and anti-apoptotic properties
*Inflam↓,
*antiOx↑,
*Risk↓, UA’s therapeutic potential in CNS disorders, such as Alzheimer’s disease, Parkinson’s disease, and stroke.
*Aβ↓, UA enhances microglial phagocytosis of Aβ plaques, suppresses neuroinflammation, and reduces tau hyperphosphorylation by restoring mitophagy to eliminate abnormal mitochondria
*p‑tau↓,
*p62↓, In doxorubicin-induced cardiomyopathy mice, UA upregulates p62, LC3-II, PINK1, and Parkin expression, restoring impaired mitophagy, mitigating membrane potential loss and ROS accumulation,
*PARK2↑,
*MMP↑,
*ROS↓,
*Strength↑, Randomized controlled trials in healthy middle-aged and older adults show that oral supplementation with 500–1000 mg of UA significantly improves skeletal muscle endurance and mitochondrial efficiency, reduces plasma inflammatory markers (such as C-r
*CRP↓,
*IL1β↓, UA activates sirtuin 1 (SIRT1)-mediated deacetylation of NF-κB p65, suppressing glial cell activation and the production of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α)
*IL6↓,
*TNF-α↓,
*AMPK↑, UA enhances brain adenosine 5′-monophosphate-activated protein kinase (AMPK) activation, attenuating NF-κB and MAPK activity, mitigating neuroinflammation, and supporting synaptic recovery
*NF-kB↓,
*MAPK↓,
*p62↑, In a renal ischemia-reperfusion injury model, UA activates the p62—kelch-like ECH-associated protein 1 (Keap1)—nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, boosting superoxide dismutase and catalase activity while lowering ROS levels
*NRF2↑,
*SOD↑,
*Catalase↑,
*HO-1↑, UA upregulates the Keap1-Nrf2/heme oxygenase 1 (HO-1) pathway to inhibit ferroptosis and reduce lipid peroxide accumulation in lung tissue
*Ferroptosis↓,
*lipid-P↓,
*Cartilage↑, reducing cartilage degradation and synovial inflammation
*PI3K↓, UA suppresses the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) and Akt/IκB kinase (IKK)/NF-κB signaling pathways, reducing neuronal apoptosis while enhancing BBB integrity and neurological outcomes
*Akt↓,
*mTOR↓,
*Apoptosis↓,
*neuroP↑,
*Bcl-2↓, cerebral artery occlusion model, UA treatment lowers Bcl-2 expression and elevates Bcl-2 associated X protein (Bax) and caspase-3 levels
*BAX↑,
*Casp3↑,
*ATP↑, UA restores mitochondrial membrane potential and ATP production in cardiomyocytes, balancing carnitine palmitoyltransferase1-dependent fatty acid oxidation to reduce apoptosis
*eff↑, in humanized homozygous amyloid beta knockin mice modeling late-onset AD, UA combined with green tea extract (Epigallocatechin gallate) more effectively reduces brain Aβ40 and Aβ42 levels compared to UA alone [106].
*motorD↑, UA administration elevated striatal dopamine levels and enhanced motor coordination, accompanied by suppression of NLRP3 inflammasome activation
*NLRP3↓,
*radioP↑, In a radiation-induced primary astrocyte model, UA activated the PINK1/Parkin-mediated mitophagy pathway, significantly reducing ROS levels in both cells and mitochondria,
*BBB↑, preclinical studies showing that UA primarily crosses the mouse BBB

7887-

VT,

IVT,

Dietary Flavonoids Vitexin and Isovitexin: New Insights into Their Functional Roles in Human Health and Disease Prevention

Review,

AD,

Review,

Var,

*antiOx↑, antioxidant, anti-inflammatory, anticancer, antibacterial, and neuroprotective mechanisms.
*Inflam↓,
*AntiCan↑,
*Bacteria↓,
*neuroP↑, cardiovascular protection, blood sugar regulation, anti-obesity, anticancer, antioxidant, anti-inflammatory, and neuroprotective properties.
*Obesity↓,
*cardioP↑, Vitexin exerts a cardioprotective effect against DOX-induced cardiac toxicity by reducing oxidative stress, lowering cardiac inflammatory cytokines, increasing FOXO3a, and inhibiting caspase-3 activation.
*ROS↓, Sprague-Dawley rat hearts, H9c2 cells 10 μM Reducing ROS levels; improving mitochondrial activity, mitochondrial membrane potential, and ATP content; markedly increasing MFN2 expression and reducing the recruitment of Drp1 in mitochondria.
*MMP↑,
*ATP↑,
*MFN2↑,
*DRP1/DNM1L↓,
*FOXO3↑, Protect against DOX-induced acute cardiotoxicity Rats 30 mg/kg Vitexin induced elevated FOXO3a protein expression levels, by suppressing oxidative stress
*NRF2↑, vitexin activated nuclear factor-erythroid 2-related factor 2 (Nrf2) in HUVEC under high glucose.
*Ferroptosis↓, Diabetic nephropathy HK-2 cells/DN rat 0–40 μM Vitexin could alleviate diabetic nephropathy by attenuated ferroptosis via activating GPX4
*GPx4↑,
TumCP↓, Gastric cancer Nude mice/GC cells 2 mg/kg 10–160 μM Vitexin inhibited the malignant progression of GC in vitro and in vivo by suppressing HMGB1-mediated activation of PI3K/Akt/HIF-1α signaling pathway.
HMGB1↓,
PI3K↓,
Akt↓,
Hif1a↓,
CDK1↓, Colon cancer HCT-116 cells 1–300 μM Inhibit colon cancer HCT-116 cell proliferation by suppressing CDK1/cyclin B expression, leading to cell cycle arrest in the G2/M phase.
CycB/CCNB1↓,
TumCCA↑,
Apoptosis↑, Isovitexin Colon cancer Promoted apoptosis and suppressed cell proliferation by activating the p53 signaling pathway.
P53↑,
NF-kB↓, Non-small cell lung cancer cells A549/ H1299 cells, nude mice 1–120 μM Suppressed NF-κB, AKT and ERK activation. [24] Vitexin A549 cells, nude mice 0–40 μM Reduced the levels of p-PI3K, p-Akt, and p-mTOR.
ERK↓,
p‑PI3K↓,
miR-34a↑, Isovitexin Hepatocarcinoma SK-Hep-1 cells Mediated miR-34a upregulation induces apoptosis and suppresses the stemness of SK-SC.
Apoptosis↑,
CSCs?,
*MAPK↓, Isovitexin Acute lung injury RAW 264.7 cells 0–50 μM Inhibiting MAPK and NF-κB and activating HO-1/Nrf2 pathways.
*HO-1↑,
*hepatoP↑, EAH mice 5 mg/kg Vitexin ameliorated hepatic injury in EAH mice through activation of the AMPK/AKT/GSK-3β pathway and upregulation of the Nrf2 gene.
*AMPK↑,
*Akt↑,
*GSK‐3β↑,
*chemoP↑, Vitexin exerts a cardioprotective effect against DOX-induced cardiac toxicity by reducing oxidative stress, lowering cardiac inflammatory cytokines, increasing FOXO3a, and inhibiting caspase-3 activation.
*Casp3↓,
*IRes↝, Vitexin and isovitexin flavonoids not only affected the absorption of peripheral glucose in insulin and non-insulin sensitive tissues but also showed the potential to restore insulin resistance in HepG2 cells by enhancing cellular uptake of glucose.
*GlucoseCon↑,
ChemoSen↑, When combined with doxorubicin (Dox), vitexin can reduce tumor growth and show synergistic effects in in vivo tests, increasing antitumor efficacy.
*GSH↑, Vitexin also increased Nrf2 expression and boosted GSH and antioxidant enzymes such as SOD, CAT, GPx, and GST.
*SOD↑,
*ATF2↑,
*GPx↑,
*GSTs↑,
*AntiAge↑, In Caenorhabditis elegans, studies have shown that vitexin and isovitexin, as putative SKN-1/Nrf2 activators, increase lifespan and support a healthy lifespan.
*Stroke↓, It has been demonstrated that vitexin protects against a cerebral ischemia/reperfusion (I/R)-induced increase in the permeability of brain endothelial cells
*AChE↓, vitexin treatment significantly inhibited acetylcholinesterase activity and markedly downregulated the expression of ace-1 and ace-2.
*ACE/ACE1↓,
*ACE2↓,
*GutMicro↑, Vitexin and isovitexin have also shown promising potential in modulating intestinal microbiota and in turn play a significant role in regulating various diseases such as overweight
*MPO↓, Vitexin can also resist Helicobacter pylori infection, which may be related to its anti-myeloperoxidase (MPO) enzyme activity and inhibition of H- and K-ATPase activity
*H+/K+-ATPase↓,
*AntiDiabetic↑, Antidiabetic Vitexin and Isovitexin Inhibits α-glucosidase/α-amylase, promotes GLUT4, modulates gut microbiota
*GLUT4↑,
*Obesity↓, Anti-obesity Vitexin Activates AMPKα, inhibits C/EBPα, FAS, activates Hedgehog signaling
*HH↓,
*RenoP↑, vitexin protects the kidneys and prevents the formation of kidney stones by inhibiting pyroptosis, apoptosis, epithelial–mesenchymal transition (EMT), and macrophage activation.
*BioAv↓, Vitexin and isovitexin have poor absorption in the gastrointestinal tract, with significant first-pass effects in the intestine (approximately 94%), stomach (30%), and liver (50%), resulting in a lower bioavailability (F) (approximately 5%).
*BioAv↝, The absorption and metabolism processes of vitexin and isovitexin in the human body are complex, and their bioavailability is influenced by multiple factors, including the action of the gut microbiota, interactions with dietary components, first-pass
*BioAv↑, The vitexin-loaded bilayer nanoparticles are designed by assembling soybean peptides and coating them with a goblet cell-targeting peptide. They significantly increase the bioaccessibility and bioavailability of vitexin

Showing Research Papers: 1 to 27 of 27

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 27

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

ACE/ACE1↓, 1, ACE2↓, 1, H+/K+-ATPase↓, 1, IRes↝, 1, Stroke↓, 2,

Redox & Oxidative Stress(tgid=1) ⓘ

4-HNE↓, 2, antiOx↑, 6, Catalase↑, 5, Ferroptosis↓, 23, GPx↑, 2, GPx4↓, 1, GPx4↑, 10, GPx4∅, 1, GSH↑, 5, GSR↓, 1, GSTs↓, 1, GSTs↑, 1, HO-1↓, 1, HO-1↑, 6, HO-1↝, 1, HO-1∅, 1, Iron↓, 1, i-Iron↓, 2, lipid-P↓, 6, lipid-P↑, 1, MDA↓, 6, MFN2↑, 1, MPO↓, 1, NRF2↓, 1, NRF2↑, 13, NRF2∅, 1, PARK2↑, 1, ROS↓, 11, mt-ROS↓, 1, SOD↑, 8, TAC↑, 1, xCT/SLC7A11↑, 2,

Metal & Cofactor Biology(tgid=2) ⓘ

Ferritin↑, 1, FTH1↑, 1, IronCh↑, 2, NCOA4↝, 1, TfR1/CD71↓, 2,

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 2, DRP1/DNM1L↓, 1, MMP↑, 2, mtDam↓, 2, PGC-1α↑, 1,

Core Metabolism/Glycolysis(tgid=4) ⓘ

12LOX↓, 1, ACSL4↓, 3, ACSL4∅, 1, ALAT↓, 1, AMPK↑, 2, p‑AMPK↑, 1, BUN↓, 1, FAO↓, 1, GlucoseCon↑, 1, LDH↑, 1, NADPH↓, 1,

Cell Death(tgid=5) ⓘ

Akt↓, 1, Akt↑, 1, Apoptosis↓, 3, ATF2↑, 1, BAX↓, 1, BAX↑, 1, Bcl-2↓, 1, Casp3↓, 2, Casp3↑, 1, Cyt‑c↓, 1, Fas↓, 1, Ferroptosis↓, 23, iNOS↓, 1, JNK↓, 2, MAPK↓, 2, p38↓, 1,

Transcription & Epigenetics(tgid=7) ⓘ

other↓, 1, other↑, 1, other↝, 1,

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↓, 1, GRP78/BiP↓, 2, IRE1↓, 1, PERK↓, 1,

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↑, 1, LC3B↑, 1, MitoP↑, 1, p62↓, 2, p62↑, 1,

DNA Damage & Repair(tgid=10) ⓘ

DNMT1↓, 1, DNMTs↓, 1,

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

FOXO3↑, 1, GSK‐3β↑, 1, HH↓, 1, KLF4↑, 1, mTOR↓, 1, PI3K↓, 1, TRPM7↓, 1,

Migration(tgid=13) ⓘ

5LO↓, 1, AntiAg↑, 1, Cartilage↑, 1, CD31/PECAM-1↑, 1, NFAT↓, 1, PKCδ↑, 1,

Angiogenesis & Vasculature(tgid=14) ⓘ

ATF4↓, 1, NO↓, 1, TXA2↓, 1,

Barriers & Transport(tgid=15) ⓘ

BBB↑, 4, GLUT4↑, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 2, CRP↓, 1, IL17↓, 1, IL1β↓, 3, IL6↓, 2, Inflam↓, 10, NF-kB↓, 2, PGE2↓, 1, TLR4↓, 1, TNF-α↓, 4,

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 2, BDNF↑, 1, p‑tau↓, 1,

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 2, NLRP3↓, 1,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 2, BioAv↑, 3, BioAv↝, 3, eff↓, 1, eff↑, 4,

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1, AST↓, 1, BloodF↑, 1, BP↓, 1, creat↓, 1, CRP↓, 1, Ferritin↑, 1, GutMicro↑, 1, IL6↓, 2, LDH↑, 1,

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1, AntiCan↑, 1, AntiDiabetic↑, 1, cardioP↑, 6, chemoP↑, 1, cognitive↑, 3, hepatoP↑, 2, memory↑, 2, motorD↑, 1, neuroP↑, 6, Obesity↓, 2, radioP↑, 1, RenoP↑, 5, Risk↓, 1, Strength↑, 1, toxicity↓, 1, Wound Healing↑, 1,

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1, Sepsis↓, 2,
Total Targets: 155

Scientific Paper Hit Count for: Ferroptosis, Ferroptosis

3 Baicalein
3 Rosmarinic acid
2 doxorubicin
2 Berberine
2 Shikonin
2 Selenite (Sodium)
1 3-bromopyruvate
1 cetuximab
1 Artemisinin
1 Luteolin
1 Cisplatin
1 Carvacrol
1 Chlorogenic acid
1 Curcumin
1 Dipyridamole
1 Formononetin
1 Hydrogen Gas
1 Hyperoside
1 Isoliquiritigenin
1 isoquercitrin
1 Piperlongumine
1 Silymarin (Milk Thistle) silibinin
1 Urolithin
1 Vitexin
1 Isovitexin

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:114  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

Ferroptosis Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Metal & Cofactor Biology(tgid=2) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Synaptic & Neurotransmission(tgid=18) ⓘ

Protein Aggregation(tgid=19) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

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