Cartilage Cancer Research Results

Cartilage, Cartilage: Click to Expand ⟱

Source:

Type:

Cartilage is a flexible connective tissue found in multiple areas of the body, including joints, the ear and nose, and intervertebral discs.
The most common type of arthritis, osteoarthritis involves wear-and-tear damage to a joint's cartilage.
Chondrosarcoma is a rare type of bone cancer that develops in cartilage cells.
Cartilage Degradation: Cancer can lead to the degradation of cartilage, particularly in joint-related cancers. This degradation can result in pain and loss of function, impacting the patient's quality of life.
Biomarkers: Specific proteins and genes associated with cartilage metabolism (e.g., collagen types, aggrecan, and matrix metalloproteinases) can serve as biomarkers for cancer diagnosis and prognosis. Their expression levels may indicate the presence of malignancy or the aggressiveness of a tumor.

Scientific Papers found: Click to Expand⟱

5988-

Chit,

Chitosan immunomodulation: insights into mechanisms of action on immune cells and signaling pathways

Review,

Var,

DDS↑, various biomedical applications, including drug delivery, cartilage repair, wound healing, and tissue engineering, because of its unique physicochemical properties.
*Cartilage↑,
*Wound Healing↑,
Imm↑, investigation of the immunomodulatory properties of chitosan, since the biopolymer has been shown to modulate the maturation, activation, cytokine production, and polarization of dendritic cells and macrophages
cGAS–STING↑, Several signaling pathways, including the cGAS–STING, STAT-1, and NLRP3 inflammasomes, are involved in chitosan-induced immunomodulation. CS activates the cGAS–STING signaling pathway
STAT1↑, One crucial factor is DDA, as it was observed that 80% DDA CS activated the STAT-1 pathway, whereas 98% DDA did not
NLRP3↑, activation of the NLRP3 inflammasome by CS requires the presence of mitochondrial ROS.
*DCells↑, CS has been studied for its potential impact on DC activation, which is a crucial step in initiating the immune response.
*IL10↓, The use of CS also reduced IL-10 production and increased TGF-β1, TNF-α, and interleukin-1 beta (IL-1β) (p < 0.001) levels.
*TGF-β1↓,
*TNF-α↓,
IL1β↓,
ROS↑, CS internalization in DCs caused mitochondrial stress and led to the production of reactive oxygen species (ROS)

4111-

MF,

Coupling of pulsed electromagnetic fields (PEMF) therapy to molecular grounds of the cell

Review,

Arthritis,

*Inflam↓, ultimately lead to a dampening of inflammatory signals like interleukins
*Cartilage↑, this therapy has positive effects for the regeneration of musculoskeletal tissues such as cartilage, bone, tendon and ligament
*Pain↓, Ryang We et al. [18] found a significant beneficial effect of PEMF on WOMAC pain scores at 1 month compared with a sham treatment
*QoL↑, significant improvements in mobility, daily activity score as well as global score during treatment of acute osteoarthritis of knee joint
*Dose↝, PEMF stimulation (38 Hz, 2 mT) for 2 h per day enhanced osteoblastic functions through amelioration of the cytoskeletal organization;
*VEGF↑, increase of anti-inflammatory prostaglandins, and a huge rise in the Vascular Endothelial Growth Factor (VEGF)-A-mRNA transcription.
*NO↑, stimulatory effect of PEMF on osteoblast proliferation and differentiation is accompanied by an increase in nitric oxide (NO) synthesis
*TGF-β↑, Transforming Growth Factor (TGF-β) family is enhanced by PEMF[67] and local expression of TGF-β results in improved bone fracture healing
*MMP9↓, PEMF treatment suppressed IL-1β-mediated up-regulation of MMP-9 protein levels.
*PGE2↑, Sontag and Dertinger [97] investigated the liberation of prostaglandin E2 (PGE2) during application of EMF of different frequencies: here “windows” at 6 and 16 Hz were found, where PGE was 200% above 0 Hz baseline.
*GPx3↑, PEMF exposure also induced expression of GPX3, SOD2, CAT and GSR on mRNA, protein and enzyme activity level
*SOD2↑,
*Catalase↑,
*GSR↑,
*Ca+2↑, many EMF-effect studies is a direct action on voltage-gated calcium channels (VGCCs) (Figure 1). This is normally accompanied by a rapid increase of Ca2+

3566-

MF,

Positive and Negative Effects of Administering a Magnetic Field to Patients with Rheumatoid Arthritis (RA)

Study,

Arthritis,

39 patients with RA, who were randomly assigned to two groups: SMF—static magnetic field (n = 18) and PEMF

*Inflam↓, Magnetotherapy applied to patients with rheumatoid arthritis (RA) produces anti-inflammatory, analgesic and antioedema effects.
*QoL↑, findings show improved functional status by 0.26 points on average (p = 0.0166) measured with the Health Assessment Questionnaire (HAQ-20),
*Pain↓, reduced pain by 2.2 points on average (p = 0.0000) on the Visual Analogue Scale (VAS)
*motorD↑, decreased duration of morning stiffness by 23.2 min on average (p = 0.0010) and reduced severity of morning stiffness by 15.2 points on average. entire group showed an increase in the range of motion in the joints of the dominant hand by 1.9 mm on av
*toxicity↓, Magnetotherapy, being a non-thermal method, is safe and rarely causes negative effects
*Cartilage↑, it slows down degenerative processes in the porcine articular cartilage.
*Inflam↓, Conversely, in the PEMF group, the hand volume decreased by as much as 19.5 mm3 on average and the change was statistically significant.

193-

MFrot,

MF,

Rotating Magnetic Field Mitigates Ankylosing Spondylitis Targeting Osteocytes and Chondrocytes via Ameliorating Immune Dysfunctions

in-vivo,

Arthritis,

 Ankylosing Spondylitis arthritis:  Mouse model

BMD↑, loss reduced
Cartilage↑, more intact cartilage surfaces and denser proteoglycan
IL17↓,
IL22↓,
IL23↓,
IL28↓,
CD4+↓, tremendously attenuated
CD8+↓, In this investigation, data showed that RMF treatment decreased CD3-expressing proliferative cells via immunostaining and reduced CD4+/CD8+ T-cells via flow cytometry in AS mice
LAMB3↑,
COL4↓,
THBS2↓,
ITGA11↓,
PPARγ↑, mice have decreased expression of peroxisome proliferator-activated receptor γ (PPAR-γ), a ligand-activated transcription factor belonging to the nuclear hormone receptor superfamily, which RMF reverses.
ACAA1↓,
PLIN1↓,
FABP4↓,
PCK1↓,
UCP1↓,
TNF-α↓,

3847-

MSM,

Methylsulfonylmethane: Applications and Safety of a Novel Dietary Supplement

Review,

Arthritis,

*Inflam↓, common use as an anti-inflammatory agent
*Pain↓, A variety of health-specific outcome measures are improved with MSM supplementation, including inflammation, joint/muscle pain, oxidative stress, and antioxidant capacity.
*ROS↓,
*antiOx↑,
*Dose↝, MSM is well-tolerated by most individuals at dosages of up to four grams daily, with few known and mild side effects
*Half-Life↝, Pharmacokinetic studies indicate that MSM is rapidly absorbed in rats [63,64] and humans [65], taking 2.1 h and <1 h, respectively.
*NF-kB↓, The inhibitory effect of MSM on NF-κB results in the downregulation of mRNA for interleukin (IL)-1, IL-6, and tumor necrosis factor-α (TNF-α) in vitro
*IL1↓,
*IL6↓,
*TNF-α↓,
*iNOS↓, MSM can also diminish the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) through suppression of NF-κB;
*COX2↓,
*NLRP3↓, MSM negatively affects the expression of the NLRP3 inflammasome by downregulating the NF-κB production of the NLRP3 inflammasome transcript and/or by blocking the activation signal in the form of mitochondrial generated reactive oxygen species (ROS)
*NRF2↑, MSM influences the activation of at least four types of transcription factors: NF-κB, signal transducers and activators of transcription (STAT), p53, and nuclear factor (erythroid-derived 2)-like 2 (Nrf2).
*STAT↓, MSM has been shown to repress the expression or activities of STAT transcription factors in a number of cancer cell lines in vitro
*Cartilage↑, , in vitro studies suggest that MSM protects cartilage through its suppressive effects on IL-1β and TNF-α
*eff↑, Supplementation with glucosamine, chondroitin sulfate, MSM, guava leaf extract, and Vitamin D improved physical function in patients with knee osteoarthritis based on the Japanese Knee OA Measure
*eff↑, MSM in combination with boswellic acid was also shown to improve knee joint function as assessed through the Lequesne Index
*GSH↑, MSM is able to restore the reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio to normal levels, decrease NO production, and reduce neuronal ROS production following HIV-1 Tat exposure
*uricA↓, Humans studies show promise for MSM as an antioxidant with similar results noted, including reductions in MDA [19,167,168], protein carbonyls (PC) [167,168], and uric acid [168] and increases in GSH [167] and TEAC [159,161,168].
tumCV↓, MSM independently has been shown to be cytotoxic to cancer cells by inhibiting cell viability through the induction of cell cycle arrest [119,122,123], necrosis [119], or apoptosis
TumCCA↑,
necrosis↑,
Apoptosis↑,
VEGF↓, reduced expression of oncogenic proteins such as vascular endothelial growth factor (VEGF) [99,100,101,123], heat shock protein (HSP)90α [100], and insulin-like growth factor-1 receptor (IGF-1R)
HSP90↓,
IGF-1?,

3931-

PTS,

Pterostilbene Protects against Osteoarthritis through NLRP3 Inflammasome Inactivation and Improves Gut Microbiota as Evidenced by In Vivo and In Vitro Studies

in-vivo,

Arthritis,

OA mouse

*Inflam↓, pterostilbene (PT), a natural anti-inflammatory substance, for its protective effects and safety during prolonged use on OA
*NLRP3↓, PT reduced NLRP3 inflammation activation
*GutMicro↑, PT also altered gut microbiota by reducing inflammation-associated flora and increasing the abundance of healthy bacteria in OA groups.
*lipid-P↓, reducing lipid accumulation and inflammation
*ROS↓, PT has been found to inhibit ROS generation and inflammation, exerting an antiarthritic effect on rheumatoid arthritis (RA)
*Cartilage↑, PT Ameliorates the Cartilage Matrix Loss and the Joint Damage in the OCP-Induced OA Model
*IL6↓, PT Inhibits IL-1β-Induced IL-6 Production and Prevents Cartilage Extracellular Matrix Degradation in SW1353 Cells
*MMP13↓, PT Inhibits LPS/ATP-Stimulated NLRP3 Inflammasome Activation and MMP-13 Production in THP-1 Cells
*Dose↝, In human adults, PT can be safely consumed up to 250 mg per day without damaging any vital organs, such as the liver and kidney

3933-

RT,

The Pharmacological Potential of Rutin

Review,

AD,

Review,

Stroke,

Review,

Arthritis,

*antiOx↑, it has demonstrated a number of pharmacological activities, including antioxidant, cytoprotective, vasoprotective, anticarcinogenic, neuroprotective and cardioprotective activities
*neuroP↑,
*cardioP↑, cardioprotective effect is due to the virtue of the antioxidant effect of rutin
*Inflam↓, Reduction of ‘neuroinflammation’ in rat model of ‘sporadic dementia of Alzheimer type’ (Javed et al., 2012) and neuroprotective effects in ‘dexamethasone-treated mice’ (Tongjaroenbuangam et al., 2011) were observed on rutin administration.
*TNF-α↓, Rutin suppressed activity of proinflammatory cytokines by diminishing TNF-α and IL-1β production in microglia.
*IL1β↓,
*IL8↓, Rutin caused attenuation of streptozotocin-induced inflammation by decreasing the activity of the glial fibrillary acidic protein, interleukin-8, cyclooxygenase-2, inducible nitric oxide synthase and nuclear factor-kB
*COX2↓,
*iNOS↓,
*NF-kB↓,
*cognitive↑, useful in averting cognitive deficits and proves to be beneficial in the treatment of ‘sporadic dementia of Alzheimer type’
*Cartilage↑, rutin slowed down inflammatory and catabolic cartilage markers in osteoarthritic lesions in the Hartley guinea pig
*AntiAg↑, Rutin in vitro caused concentration-dependent inhibition of platelet activating factor induced washed rabbit platelet aggregation
*ROS↓, Rutin inhibits osteoclast formation by decreasing oxygen reactive species and TNF-alpha by inhibiting activation of NF-kappaB (
*lipid-P↓, Rutin significantly decreased oxaliplatin-induced peroxidative changes in the spinal cord and lipid peroxidation along with inducible nitric oxide
*hepatoP↑, Rutin is extensively studied for hepatoprotective activity in experimental animals
*ALAT↓, Administration of rutin caused a decrement in levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and gamma-glutamyl transpeptidase in serum raised due to carbon tetrachloride.
*AST↓,
*RenoP↑, Administration of rutin caused a decrement in levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and gamma-glutamyl transpeptidase in serum raised due to carbon tetrachloride.

5336-

TFdiG,

Theaflavin-3,3′-Digallate Protects Cartilage from Degradation by Modulating Inflammation and Antioxidant Pathways

in-vivo,

Nor,

rats

*IL6↓, TFDG was found to inhibit proinflammatory factors (IL-6, TNF-α, iNOS, and PGE)
*TNF-α↓,
*iNOS↓,
*PGE1↓,
*ROS↓, TFDG accelerated the scavenging of ROS caused by IL-1β a
*Inflam↓, TFDG suppressed the PI3K/AKT/NF-κB and MAPK signaling pathways to delay the inflammatory process.
*PI3K↓,
*Akt↓,
*NF-kB↓,
*MAPK↓,
*Cartilage↑, TFDG could protect cartilage from degradation and alleviate osteoarthritis in rats, which suggests that TFDG has potential as a drug candidate for OA therapy.

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

4875-

Uro,

Impact of the Natural Compound Urolithin A on Health, Disease, and Aging

Review,

AD,

Review,

Stroke,

Review,

ostP,

Review,

IBD,

*MitoP↓, Experimental models consistently show that UA increases mitophagy and mitochondrial function and blunts excessive inflammatory responses.
*Strength↑, UA is a promising strategy to target health and disease conditions of aging, especially those linked to mitochondrial and muscle dysfunction.
*PINK1↑, UA can activate. PTEN-induced kinase 1 (PINK1)/Parkin-dependent mitophagy starts with the stabilization of the kinase PINK1,
*PARK2↑, which recruits and phosphorylates the ubiquitin-conjugating protein Parkin.
*Inflam↓, anti-inflammatory effect of UA was reported for the first time as a decrease in mRNA and protein levels of the inflammatory marker cyclooxygenase 2 (COX2)
*COX2↓,
*IL1β↓, In neuronal tissues, UA treatment reduced levels of IL-1β, IL-6, and TNFα in the brains of the amyloid precursor protein/presenilin 1 (APP/PS1) mouse model of AD
*IL6↓,
*TNF-α↓,
*OS↑, impact on worm longevity showed that UA extends lifespan by 45%,
*cardioP↑, reduction in IRI markers, such as circulating creatine kinase and lactate dehydrogenase levels, and by fewer apoptotic cells in the heart
*memory↑, Increased learning, memory retention, neuronal survival, and neurogenesis in the hippocampus was achieved with UA administration in the APP/PS1 mouse model of AD
*neuroG↑,
*neuroP↑, UA was shown to have neuroprotective effects in the EAE mouse model of multiple sclerosis (MS)
*Cartilage↑, In a model of osteoarthritis, an age-related and disabling joint disease caused by a slow degeneration of cartilage,
*Inflam↓, UA has protective effects against a chronic DSS-induced model of IBD, leading to reduced levels of colon inflammation markers and to better mucosal integrity.
*RenoP↑, UA consistently reduced tubular damage induced by cisplatin, as shown by histopathology and by a reduction in circulating markers of kidney damage
*eff↑, When administered as nanoparticles to increase its bioavailability, UA even improved the survival of mice that received a lethal dose of cisplatin
*Dose↝, UA showed a favorable safety profile, with no observed side effects following either single oral administration of UA up to 2000 mg or multiple oral dosing (28 days) of UA up to 1000 mg daily.
*Half-Life↑, It showed a relatively long-half life (t1/2 = 17–22 hours),
*NRF2↑, Other mechanisms of action have been proposed for UA, such as the activation of the Ahr/Nrf2 pathway and its downstream antioxidative stress response
*GutMicro↑, A recent report also showed an impact of direct UA supplementation on gut microflora in obese rats

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:

Infection & Microbiome ⓘ

CD8+↓, 1,
Total Targets: 33

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 3, Catalase↑, 2, Ferroptosis↓, 1, GPx3↑, 1, GSH↑, 1, GSR↑, 1, HO-1↑, 1, lipid-P↓, 3, NRF2↑, 3, PARK2↑, 2, ROS↓, 5, SOD↑, 1, SOD2↑, 1, uricA↓, 1,

Mitochondria & Bioenergetics ⓘ

ATP↑, 1, MMP↑, 1, PINK1↑, 1,

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1, AMPK↑, 1,

Cell Death ⓘ

Akt↓, 2, Apoptosis↓, 1, BAX↑, 1, Bcl-2↓, 1, Casp3↑, 1, Ferroptosis↓, 1, iNOS↓, 3, MAPK↓, 2,

Autophagy & Lysosomes ⓘ

MitoP↓, 1, MitoP↑, 1, p62↓, 1, p62↑, 1,

Proliferation, Differentiation & Cell State ⓘ

mTOR↓, 1, neuroG↑, 1, PI3K↓, 2, STAT↓, 1,

Migration ⓘ

AntiAg↑, 1, Ca+2↑, 1, Cartilage↑, 9, MMP13↓, 1, MMP9↓, 1, TGF-β↑, 1, TGF-β1↓, 1,

Angiogenesis & Vasculature ⓘ

NO↑, 1, VEGF↑, 1,

Barriers & Transport ⓘ

BBB↑, 1,

Immune & Inflammatory Signaling ⓘ

COX2↓, 3, CRP↓, 1, DCells↑, 1, IL1↓, 1, IL10↓, 1, IL1β↓, 3, IL6↓, 5, IL8↓, 1, Inflam↓, 10, NF-kB↓, 4, PGE1↓, 1, PGE2↑, 1, TNF-α↓, 6,

Synaptic & Neurotransmission ⓘ

p‑tau↓, 1,

Protein Aggregation ⓘ

Aβ↓, 1, NLRP3↓, 3,

Drug Metabolism & Resistance ⓘ

Dose↝, 4, eff↑, 4, Half-Life↑, 1, Half-Life↝, 1,

Clinical Biomarkers ⓘ

ALAT↓, 1, AST↓, 1, CRP↓, 1, GutMicro↑, 2, IL6↓, 5,

Functional Outcomes ⓘ

cardioP↑, 2, cognitive↑, 1, hepatoP↑, 1, memory↑, 1, motorD↑, 2, neuroP↑, 3, OS↑, 1, Pain↓, 3, QoL↑, 2, radioP↑, 1, RenoP↑, 2, Risk↓, 1, Strength↑, 2, toxicity↓, 1, Wound Healing↑, 1,
Total Targets: 85

Scientific Paper Hit Count for: Cartilage, Cartilage

3 Magnetic Fields
2 Urolithin
1 chitosan
1 Magnetic Field Rotating
1 Methylsulfonylmethane
1 Pterostilbene
1 Rutin
1 Aflavin-3,3′-digallate

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

Cartilage Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Cellular Microenvironment ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Autophagy & Lysosomes ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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