Target intelligence / Profile preview

Oxidative stress signaling

Molecular classification
Signaling pathway/network, Transcription factors (e.g., NRF2, FoxO, p53), Kinases (e.g., MAPK: ERK, JNK, p38), Enzymes (e.g., SOD, GPX, CAT, PRX), Redox sensors (KEAP1, thioredoxin)
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Overview

Oxidative stress signaling describes the cellular sensing and response network to increased reactive oxygen species, coordinating antioxidant defense, repair, apoptosis, and cell fate decisions via interconnected pathways such as MAPK, NRF2–KEAP1, FoxO, and p53. Dysfunctional or excessive signaling contributes to disease progression in cancer, neurodegeneration, cardiovascular and metabolic disorders. It is not a direct molecular target but comprises actionable nodes for therapeutic intervention.

Other names
oxidative stress pathwayredox signalingROS signaling
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Mechanism of action

Drugs typically act by: Activating antioxidant pathways (NRF2 signaling); Modulating kinase pathways (MAPK signaling: inhibiting ERK, activating p38 or JNK); Scavenging or reducing ROS (antioxidants); Regulating mitochondrial ROS production.

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Biological functions

Regulation of antioxidant defensesSignal transductionApoptosisCell survivalCell proliferationImmune responseMitochondrial function and energy metabolismStress adaptation
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Disease associations

CancerCardiovascular diseaseNeurodegenerative diseaseInflammationDiabetes and metabolic disordersAging
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Safety considerations

Redox imbalance (pro-oxidant or overactive antioxidant effects)Off-target effects due to broad pathway involvementPotential for impaired cell signaling or apoptosis (with indiscriminate ROS suppression)
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Interacting drugs

NRF2 activators (e.g., bardoxolone)

3 more in the full profile.

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Biomarkers

Superoxide dismutase (SOD) activityMyeloperoxidase (MPO) activityGlutathione (GSH) levels3-chlorotyrosine (3-Cl-Tyr)Malondialdehyde (MDA) (indicative of lipid peroxidation)

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