Oxidative Stress – Associated Diseases & Conditions

Oxidative stress is implicated in the pathogenesis of a wide range of chronic diseases. This document outlines key conditions linked to oxidative stress, the mechanisms involved, and supporting evidence.

Disease / ConditionRole of Oxidative Stress in PathogenesisNotes / Evidence
AtherosclerosisOxidized LDL triggers macrophage activation, foam cell formation, and vascular inflammation, promoting plaque buildup.ROS-mediated lipid oxidation is a hallmark; antioxidants show partial protection in studies.
HypertensionROS reduce nitric oxide availability, leading to endothelial dysfunction and increased vascular tone.NADPH oxidase overactivity documented in hypertensive patients.
Diabetes Mellitus & ComplicationsHyperglycemia increases ROS production, damaging beta cells, promoting insulin resistance, and worsening microvascular damage.Elevated oxidative stress markers found in diabetic patients with nephropathy, retinopathy, neuropathy.
Neurodegenerative Diseases (Alzheimer’s, Parkinson’s, ALS)ROS damage neuronal membranes, DNA, and promote misfolding/aggregation of proteins like amyloid-beta and alpha-synuclein.Oxidative damage markers elevated in brain tissue and CSF of affected patients.
CancerROS cause DNA mutations and promote pro-survival signaling; chronic inflammation fosters tumor progression.Both carcinogenesis and tumor suppression roles depending on ROS level.
Chronic Kidney DiseaseROS contribute to glomerular and tubular injury, accelerate fibrosis, and worsen renal function decline.Increased F2-isoprostanes and protein carbonyls seen in CKD patients.
COPD & Respiratory DiseasesCigarette smoke and pollutants increase ROS burden in lung tissue, activating inflammatory pathways.High oxidative stress linked with severity of airway remodeling.
Rheumatoid ArthritisROS contribute to synovial inflammation, cartilage degradation, and bone erosion.Oxidative stress biomarkers elevated in synovial fluid and serum of RA patients.
AgingCumulative oxidative damage to DNA, proteins, and lipids drives functional decline over time.Free radical theory of aging partially supported by experimental data.