Oxidative Stress–Inflammation–Fibrosis Axis in Chronic Liver Diseases
Keywords:
oxidative stress, inflammation, hepatic fibrosis, hepatocyte death, stellate cells, NLRP3 inflammasome, NAFLD/NASH, cirrhosisAbstract
Chronic liver diseases share converging biochemical processes driven by oxidative stress, innate immune activation, and maladaptive wound‑healing, culminating in fibrosis and cirrhosis. Reactive oxygen species generated by mitochondrial dysfunction, cytochrome P450 enzymes, and NADPH oxidases modify lipids and proteins, triggering hepatocyte injury and death with release of danger signals and lipid peroxidation products that amplify inflammatory cascades. Pattern‑recognition receptors activate NF‑κB and NLRP3 inflammasomes, promoting cytokine production, pyroptosis, and recruitment of immune cells that further perpetuate oxidative damage and inflammation. These events synergistically activate hepatic stellate cells and portal fibroblasts, driving extracellular matrix deposition, architectural distortion, and ultimately portal hypertension and liver failure. Understanding this oxidative stress–inflammation–fibrosis axis offers an integrated framework to link biochemical markers with molecular pathogenesis and to identify therapeutic targets aimed at interrupting profibrogenic signaling.
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