diuretic Cancer Research Results

diuretic, diuretic: Click to Expand ⟱

Source:

Type:

diuretic is a substance that makes the body produce and excrete more urine.

| Use                                   | Why diuretics help                                     |
| ------------------------------------- | ------------------------------------------------------ |
| High blood pressure                   | Lower fluid volume, reducing pressure in blood vessels |
| Edema / swelling                      | Remove excess fluid from tissues                       |
| Heart failure                         | Reduce fluid overload                                  |
| Kidney or liver-related fluid buildup | Help manage retained fluid                             |

Scientific Papers found: Click to Expand⟱

6348-

DRE,

New prospects in oncotherapy: bioactive compounds from Taraxacum officinale

Review,

Var,

Dose↝, Key bioactive compounds, such as taraxasterol, chlorogenic acid, chicoric acid, and taraxinic acid, have been identified as promising agents capable of inhibiting tumor cell proliferation and modulating oncogenic pathways.
TumCP↓,
toxicity↓, Given its multi-target biological activity and low toxicity, Taraxacum officinale holds significant potential for integration into oncotherapy as an adjuvant treatment.
*AntiDiabetic↑, reported to exhibit a broad spectrum of pharmacological effects, including antidiabetic, antioxidant, hepatoprotective, diuretic, anti-inflammatory, neuroprotective, antidepressant, antimicrobial, and immunostimulant properties
*antiOx↑,
*hepatoP↑,
*diuretic↑,
*Inflam↓,
*neuroP↑,
*Imm↑,
eff↑, Innovative formulations such as silver nanoparticles synthesized using aqueous leaf extracts (TOL-AgNPs) demonstrated enhanced cytotoxicity, achieving 95% inhibition of HepG2 cell proliferation at 200 μg/mL
Apoptosis↑, Figure 1
tumCV↓,
selectivity↑,
TumCMig↓, taraxasterol inhibits papillary thyroid cancer cell migration and prevents epithelial-mesenchymal transition (EMT) induced by TGF-β by decreasing the expression of matrix metalloproteinases MMP-2 and MMP-9 and blocking the Wnt/β-catenin signaling pa
EMT↓,
MMP2↓,
MMP9↓,
Wnt↓,
β-catenin/ZEB1↓,
PI3K↓, regulation of key signaling pathways such as PI3K/Akt, JNK, and ERK1/2.
Akt↓,
JNK↓,
ERK↓,

6365-

DRE,

AN OVERVIEW OF THERAPEUTIC POTENTIALS OF TARAXACUM OFFICINALE (DANDELION): A TRADITIONALLY VALUABLE HERB WITH A REACH HISTORICAL BACKGROUND

Review,

Var,

*Inflam↓, including anti-inflammatory, anti-tumor, immunostimulatory, anti-microbial, anti-viral, anti-oxidant, anti-diabetic, geno-protective, diuretic and kidney-protective, hepato-protective, neuro-protective
*AntiTum↑,
*Imm↑,
*antiOx↑,
*AntiDiabetic↑,
*diuretic↑,
*RenoP↑,
*hepatoP↑,
*neuroP↑,
AntiTum↑, In 1981, for the first time, it was shown that the hot water extract of dandelion possessed anti-tumor activity
TNF-α↑, It induces apoptotic cell death by raising the production of tumor necrosis factor (TNF)-α and interleukin (IL)-1α
IL1β↑,
Apoptosis↑, The TNF-α and IL-1α are two potent inducers of cancer cell apoptosis
MMP2↓, dampening the activities of matrix metallopro- teinases (MMPs) such as MMP-2 and MMP-9
MMP9↑,
eff↑, Combination treatment with TRAIL targeting and dandelion resulted in TRAIL-induced apoptosis mediated through inhibition of the MKK7-TIPRL interaction and subsequent ac- tivation of MKK7-JNK phosphorylation.
Diff↑, The differentiation-inducing effects of dandelion on the human leukemia cell line (HL60) and a B16 mouse melanoma-derived sub-clone with high differentiation capability (B16 2F2) were investigated
*ROS↓, Both cell viability and ROS assays confirmed that extract effectively attenuated glutamate-induced cytotoxicity and ROS generation.
*HO-1↑, Moreover, extract increased the expression of HO-1 and promoted the nuclear translocation of nuclear factor erythroid 2-relat- ed factor-2 (Nrf2).
*NRF2↑,
*lipid-P↓, andelion can improve lipid metabolism and is advantageous in preventing diabetic complica- tions from lipid peroxidation and free radicals in diabetic rats124

6366-

DRE,

A comprehensive review of the benefits of Taraxacum officinale on human health

Review,

Var,

*diuretic↑, These properties are diuretic, hepatoprotective, anticolitis, immunoprotective, antiviral, antifungal, antibacterial, antiarthritic, antidiabetic, antiobesity, antioxidant and anticancer effects
*hepatoP↑,
*Imm↑,
*Bacteria↓,
*AntiArt↑,
*AntiDiabetic↑,
*Obesity↓,
*antiOx↓,
*AntiCan↑,
Dose?, The main phytochemicals are: carotenoids; flavonoids (e.g., quercetin, chrysoeriol, luteolin-7-glucoside); phenolic acids (e.g., caffeic acid, chlorogenic acid, chicoric acid); polysaccharides (e.g., inulin); sesquiterpene lactones (e.g., taraxinic a

6820-

EMD,

The Health Benefits of Emodin, a Natural Anthraquinone Derived from Rhubarb—A Summary Update

Review,

Nor,

Review,

Arthritis,

Review,

AD,

*diuretic↑, Emodin has a wide range of biological activities, including diuretic, antibacterial, antiulcer, anti-inflammatory, anticancer and antinociceptive.
*Bacteria↓,
*Inflam↓,
AntiCan↑,
TumCP↓, emodin inhibits processes of neoplasia at the stages of proliferation, invasion and angiogenesis.
TumCI↓,
angioG↓,
*toxicity↓, The results showed that administration of emodin at the doses of 20, 40, and 80 mg/kg for 12 weeks is safe and did not cause any pathophysiological disorders in major organs in mammals.
IFN-γ↑, more interferon gamma (IFN-γ), interleukin (IL)-12 and reactive oxygen species (ROS) and less IL-6, tumor necrosis factor alpha (TNF-α) and transforming growth factor beta1 (TGF-β1) in he alveolar cavity in the emodin group than those in the control
IL12↑,
ROS↑, In vitro, emodin at the dose of 20 μM had no effect on cell viability in HL-60N1, but increased ROS and decreased autophagy, and thus induced apoptosis in HL-60N2
TNF-α↓,
TNF-α↓,
TGF-β↓,
MAPK↓, Antitumor properties of emodin are associated with inhibiting the activity of tyrosine kinases, such as mitogen-activated protein kinase (MAPK), protein kinase C (PKC), factor kappa-light-chain-enhancer of activated B cells (NF-κB)
PKCδ↓,
NF-kB↓,
HER2/EBBR2↓, emodin suppresses the activity of HER-2/neu tyrosine kinase [55]; whereas, in colon cancer cells, emodin inhibits phosphorylation of vascular endothelial growth factor (VEGF)
VEGF↓,
DNAdam↑, Another antiproliferative mechanism of emodin activity involves induction of DNA damage by the ROS, whose concentration is considerably increased in the cells treated with this anthraquinone.
Necroptosis↑, emodin induces necroptosis in the cells of renal cancer (RCC), which is resistant to conventional cancer therapy, such as chemotherapy or radiotherapy.
Glycolysis↓, and also inhibits glycolysis by downregulation of GLUT1 through ROS-mediated inactivation of the phosphoinositide 3-kinases (PI3K)/AKT signaling pathway.
GLUT1↓,
PI3K↓,
Akt↓,
Casp9↑, increasing active caspase-9, active caspase-3, and bcl-2-like protein 4 (Bax) levels and downregulating Bcl-2.
Casp3↑,
BAX↑,
Bcl-2↓,
eff↑, Li et al. [61] revealed that a bifunctional molecule of β-dihydro-artemisinin-emodin has high antiproliferative activity (suppressing Ki-67 expression),
MMP2↓, Emodin effectively inhibits the expression of the angiogenic-related NF-kB factor, as well as its regulatory factors, including VEGF, MMP-2, MMP-9.
MMP9↓,
eff↑, Combinatorial therapy with emodin and thymoquinone was also efficient in attenuating migration of MCF-7 breast cancer cells, inducing apoptosis, inhibiting cell proliferation, while enhancing cytotoxicity
ChemoSen↑, For example, combination therapy using emodin and doxorubicin sensitize breast cancer cells to doxorubicin by inhibition of proliferation in the DNA damage pathway
P-gp/ABCB1↓, It was demonstrated that emodin downregulated Pgp expression, and enhanced cisplatin-induced apoptosis and DNA damage in the cancer cells
SREBP2↓, suppressing the cholesterol biosynthesis (inhibition the activity of SREBP-2 protein) and inhibiting the expression of the AKT.
eff↑, emodin combined with berberine significantly inhibited the activity of salt-inducible kinases 3 (SIK3), belonging to the AMPK-related kinases, which elevated expressions in breast cancer cells contributing to tumorigenesis.
*other↝, emodin has therapeutic potential for the treatment of various kinds of inflammation, such as pancreatitis, asthma, arthritis, atherosclerosis, myocarditis, glomerulonephritis and Alzheimer’s disease.
*COX2/PTGS2↓, Therapeutic properties of emodin in the treatment of joint inflammation are also associated with inhibition of expression of VEGF, cyclooxygenase 2 (COX-2), hypoxia-inducible factor 1 (HIF-1)α and histone deacetylase (HDAC).
*Hif1a↓,
*HDAC↓,
*tau↓, Emodin effectively prevents abnormal aggregation of tau proteins in PHFs
*PKCδ↑, emodin improved cognitive functions by activating the protein kinase C signaling pathway (PKC), attenuating oxidative stress and inflammatory response in mice with Alzheimer’s disease.
*ROS↓,
*Inflam↓,
AntiAg?,

6829-

EMD,

Molecular Mechanisms of Action of Emodin: As an Anti-Cardiovascular Disease Drug

*diuretic↑, diuretic, vasorelaxant, anti-bacterial, anti-viral, anti-ulcerogenic, anti-inflammatory, and anti-cancer effects.
*Bacteria↓,
*AntiViral↑,
*Inflam↓,
AntiCan↑,
*cardioP↑, timely overview of emodin related to the treatment of cardiovascular disease.
*NF-kB↓, graphic abstract Immunomoduation
*TNF-α↓,
*IL1β↓,
*NO↑,
*eNOS↑,
*PPARγ↑,
*Casp9↓, anti-apoptosis
*Casp3↓,
*GSDMD↓,
*Bcl-2↑,
*STAT3↑,
*ATP↑, anti-oxidant
*SOD↑,
*GSH↑,
*HDAC2↓, anti cardiac hypertrophy
*SIRT3↑,
ROS↑, anti-proliferative
PCNA↓,
P53↑,
cMyc↓,

6836-

EMD,

Emodin and the Anthraquinone Scaffold: Therapeutic Promise and Strategies to Overcome Translational Barriers

Review,

Nor,

*antiOx↑, graphic abstract
*neuroP↑,
*Inflam↓,
*hepatoP↑,
AntiTum↑,
*Bacteria↓,
*diuretic↑,
*AntiDiabetic↑,
*BioAv↝, formulation composition and herb–herb or herb–drug interactions are critical determinants of anthraquinone bioavailability and, ultimately, therapeutic outcomes.
*NF-kB↓, figure 4
*AMPK↑,
*JAK↓,
*STAT3↓,
*ROS↓, At low to moderate concentrations, particularly in models of inflammatory or oxidative tissue injury, emodin exerts net antioxidant and cytoprotective effects by lowering ROS levels, limiting lipid peroxidation, and enhancing endogenous antioxidant d
*lipid-P↓,
ROS↑, in cancer cells and other metabolically stressed conditions, the anthraquinone scaffold has been reported to act predominantly as a pro-oxidant, shifting redox homeostasis toward oxidative stress and promoting intracellular ROS accumulation,
TumCCA↑, In human colon cancer (WiDr) cells, aloe-emodin induced a pronounced G2/M arrest associated with suppression of cyclin B1, a critical regulator of mitotic entry.
CycB/CCNB1↓,
BAX↑, upregulation of Bax and Bak alongside the downregulation of anti-apoptotic members such as Bcl-2 and Bcl-xL.
Bcl-2↓,
MOMP↑, As a result, mitochondrial outer-membrane permeabilization (MOMP) is promoted, enabling cytochrome c release and subsequent apoptosome formation through association with Apaf-1.
Cyt‑c↑,
Casp9↑, Activation of initiator caspase-9 follows, triggering executioner caspases, notably caspase-3 and caspase-7, and culminating in apoptotic cell death
Casp3↑,
Casp7↑,
Apoptosis↑,
P53↑, where emodin-induced ROS accumulation and p53 activation contribute to the inhibition of pathological proliferation relevant to restenosis and atherosclerotic remodeling

7012-

Fuc,

Fucoidan: A promising natural therapeutic agent for protecting human kidney health

Review,

EC,

*RenoP↑, Fucoidan exhibits significant anti-inflammatory effects in kidney protection.
*Inflam↓,
*antiOx↑, Antioxidant properties effectively reduce oxidative stress in renal tissues.
*ROS↓,
*BloodF↑, Enhances renal function by improving blood flow and diuresis.
*diuretic↑,
*BioAv↓, High-MW fucoidans often display stronger anticoagulant and viscosity-modulating effects. However, they may have limited oral bioavailability,
*BioAv↑, whereas low- to medium-MW fractions show improved tissue penetration, more favorable absorption, and can retain potent anti-inflammatory and anti-fibrotic activities, making them attractive for chronic kidney disease applications
*MAPK↓, (LMWF) has been reported in models of renal ischemia-reperfusion injury, where it inhibits the MAPK signaling pathway and subsequently reduces inflammation and fibrosis
*ERK↑, fucoidan can activate the ERK/MAPK signaling pathway, which plays a crucial role in preserving the endothelial glycocalyx in CKD
*NLRP3↓, fucoidan attenuates NLRP3 inflammasome activation and subsequent podocyte pyroptosis, ultimately leading to improved renal function and reduced inflammation in diabetic kidney disease (DKD)
*NRF2↑, By inhibiting ROS-generating systems (e.g., NADPH oxidase) and activating Nrf2-dependent transcription of antioxidant genes, fucoidan limits mitochondrial dysfunction and prevents oxidative injury to podocytes and tubular epithelial cells
*MDA↓, fucoidan nanoparticles significantly reduced levels of malondialdehyde (MDA), a marker of lipid peroxidation and oxidative stress, while simultaneously upregulating the levels of superoxide dismutase (SOD) and glutathione peroxidase (GPx)
*SOD↑,
*GPx↑,
*Catalase↑, Altogether, fucoidan directly reduces renal oxidative stress by scavenging reactive oxygen species and upregulating endogenous antioxidant defenses (e.g., SOD, CAT, GPx) in tubular and glomerular cells, by suppressing upstream ROS generation
*lipid-P↓, fucoidan limits lipid peroxidation and DNA damage, thereby preserving podocyte integrity and tubular epithelial viability
*DNAdam↓,
*Fibrosis↓, Inhibition of fibrosis
*JAK2↓, fucoidan combats renal fibrosis is via the restriction of the JAK2/STAT3 signaling pathway.
*STAT3↓,
*uricA↓, By reducing serum uric acid levels, fucoidan significantly inhibits the activation of JAK2/STAT3, consequently decreasing the expression of key fibrotic markers such as collagen I and α-smooth muscle actin (α-SMA)
*COL1↓,
*α-SMA↓,
*SIRT1↑, fucoidan’s anti-fibrotic effects are further attributed to its activation of protective pathways such as Sirt-1, GLP-1R, and Nrf2/HO-1(
*HO-1↑,
*GLP-1R↑,
*HMGB1↓, Stimulating these protective pathways results in the inhibition of pro-fibrotic signaling cascades, including the HMGB1/RAGE/NF-κB/TGF-β1 pathway
*RAGE↓,
*NF-kB↓,
*TGF-β1↓,
*PI3K↓, Fucoidan also exhibits potential in curtailing the inflammatory processes associated with renal fibrosis through its inhibitory effects on the PI3K/Akt/NF-κB signaling cascade.
*Akt↓,
*GutMicro↑, research has elucidated the important role of gut microbiota in mediating the protective effects of fucoidan, suggesting that modulation of microbial communities may underlie its benefits in renal health
*SCFAs↑, Fucoidan’s positive impact on gut microbiota includes enhancing the production of short-chain fatty acids (SCFAs), especially butyrate, which are known to support gut integrity and overall health (
*Buty↑,
*IBI↑, Fucoidan's ability to enhance SCFA production has been linked to improved intestinal barrier integrity, a crucial factor in preventing the translocation of harmful substances into the bloodstream, which can exacerbate kidney injury
*TJ↑, Studies indicate that fucoidan can upregulate the expression of tight junction proteins, crucial for maintaining the integrity of the intestinal epithelium
*Dose↝, national approval in China for renal indications, indicate that fucoidan is generally safe at oral doses of 50–300 mg/day and up to 1–3 g/day in short‑ to mid‑term studies, with no major hematologic, hepatic, or renal toxicity reported.

7361-

HibSad,

Hibiscus sabdariffa L. - a phytochemical and pharmacological review

Review,

Var,

*Bacteria↓, Extracts showed antibacterial, anti-oxidant, nephro- and hepato-protective, renal/diuretic effect, effects on lipid metabolism (anti-cholesterol), anti-diabetic and anti-hypertensive effects among others.
*hepatoP↑,
*diuretic↑,
*LDL↓,
*antiOx↑, This might be linked to strong antioxidant activities, inhibition of α-glucosidase and α-amylase, inhibition of angiotensin-converting enzymes (ACE), and direct vaso-relaxant effect or calcium channel modulation.
*ACE/ACE1↓,
*Ca+2↝,
*toxicity↓, Hs has an excellent safety and tolerability record.
*ROS↓, The antioxidant activity of the extract is due to its strong scavenging effect on reactive oxygen and free radicals
*RenoP↑, Two studies were reported on the nephroprotective activity of Hs extracts on diabetic nephropathy in streptozotocin-induced type 1 diabetic rats

7360-

HibSad,

Inhibition of angiotensin convertin enzyme (ACE) activity by the anthocyanins delphinidin- and cyanidin-3-O-sambubiosides from Hibiscus sabdariffa

Study,

Nor,

*diuretic↑, The beverages of Hibiscus sabdariffa calyces are widely used in Mexico as diuretic, for treating gastrointestinal disorders, liver diseases, fever, hypercholesterolemia and hypertension
*BP↓, Different works have demonstrated that Hibiscus sabdariffa extracts reduce blood pressure in humans,
*ACE/ACE1↓, we demonstrated that this effect is due to angiotensin converting enzyme (ACE) inhibitor activity.

7376-

RS,

RENESE-R- polythiazide and reserpine tablet

Review,

Nor,

*BP↓, Renese (polythiazide) alone has demonstrated clinical effectiveness in lowering elevated blood pressure in patients without visible edema as well as in edematous hypertensive patients.
*BioAv↑, Polythiazide is well absorbed following oral administration with diuresis beginning approximately 2 hours later. Peak human plasma concentrations occur about 5 hours after ingestion.
*Half-Life↑, Polythiazide is removed slowly thereafter with a plasma elimination half-life of approximately 27 hours. One-fifth of the drug is recovered unchanged in human urine; the remainder is cleared via feces and as metabolites.
*BBB↑, Reserpine crosses the blood-brain barrier and the placenta, and appears in cord blood.
*diuretic↑, Since all diuretic agents may reduce serum levels of sodium, chloride, and potassium – especially with brisk diuresis or when used concurrently with steroids – patients should be observed regularly for early signs of fluid or electrolyte imbalance, a
*toxicity↝, Notify your physician if muscle weakness, cramps, nausea, or dizziness occur as these may indicate the loss of too much potassium from your body.

Showing Research Papers: 1 to 10 of 10

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 10

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

ACE/ACE1↓, 2, AntiArt↑, 1, Buty↑, 1, diuretic↑, 10, GLP-1R↑, 1, SCFAs↑, 1,

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 1, antiOx↑, 5, Catalase↑, 1, GPx↑, 1, GSH↑, 1, HO-1↑, 2, lipid-P↓, 3, MDA↓, 1, NRF2↑, 2, ROS↓, 5, SIRT3↑, 1, SOD↑, 2, uricA↓, 1,

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 1,

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1, LDL↓, 1, PPARγ↑, 1, SIRT1↑, 1,

Cell Death(tgid=5) ⓘ

Akt↓, 1, Bcl-2↑, 1, Casp3↓, 1, Casp9↓, 1, GSDMD↓, 1, MAPK↓, 1,

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 1,

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,

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

ERK↑, 1, HDAC↓, 1, HDAC2↓, 1, PI3K↓, 1, STAT3↓, 2, STAT3↑, 1,

Migration(tgid=13) ⓘ

Ca+2↝, 1, COL1↓, 1, Fibrosis↓, 1, PKCδ↑, 1, RAGE↓, 1, TGF-β1↓, 1, TJ↑, 1, α-SMA↓, 1,

Angiogenesis & Vasculature(tgid=14) ⓘ

eNOS↑, 1, Hif1a↓, 1, NO↑, 1,

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1, IBI↑, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1, HMGB1↓, 1, IL1β↓, 1, Imm↑, 3, Inflam↓, 7, JAK↓, 1, JAK2↓, 1, NF-kB↓, 3, TNF-α↓, 1,

Synaptic & Neurotransmission(tgid=18) ⓘ

tau↓, 1,

Protein Aggregation(tgid=19) ⓘ

NLRP3↓, 1,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1, BioAv↑, 2, BioAv↝, 1, Dose↝, 1, Half-Life↑, 1,

Clinical Biomarkers(tgid=22) ⓘ

BloodF↑, 1, BP↓, 2, GutMicro↑, 1, RAGE↓, 1,

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1, AntiDiabetic↑, 4, AntiTum↑, 1, cardioP↑, 1, hepatoP↑, 5, neuroP↑, 3, Obesity↓, 1, RenoP↑, 3, toxicity↓, 2, toxicity↝, 1,

Infection & Microbiome(tgid=24) ⓘ

AntiViral↑, 1, Bacteria↓, 5,
Total Targets: 83

Scientific Paper Hit Count for: diuretic, diuretic

3 Dandelion Root
3 Emodin
2 Hibiscus sabdariffa
1 Fucoidan
1 Rauwolfia serpentina/Indian Snakeroot

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#:1480  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

diuretic Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

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

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

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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