Fibrosis

Fibrosis is the formation of excessive fibrous connective tissue in an organ or tissue as a reparative or pathological response to injury. It involves accumulation of extracellular matrix proteins, particularly collagen, produced by activated fibroblasts and myofibroblasts. Chronic inflammation and ongoing tissue injury drive persistent scar formation, which can distort normal architecture and impair organ function. While fibrosis can be localized, it often progresses, and in many contexts it is only partially reversible if the underlying cause is addressed early.

Fibrosis can affect virtually any organ. The liver commonly accumulates fibrous tissue after chronic hepatitis, alcohol use, or metabolic disease, culminating in cirrhosis and portal hypertension. In the lungs, interstitial fibrosis stiffens tissue and limits gas exchange; idiopathic pulmonary fibrosis is a prototypical example. Kidney fibrosis contributes to chronic kidney disease, while cardiac fibrosis can accompany heart failure and arrhythmias. Skin involvement is characteristic of systemic sclerosis and related conditions.

Diagnosis relies on history and examination, supported by imaging and, when needed, tissue biopsy. Noninvasive liver fibrosis assessment uses elastography and serologic markers; liver biopsy remains definitive in some cases. Lung fibrosis is evaluated with high‑resolution CT and pulmonary function testing. Biomarkers and imaging help stage disease and monitor progression.

Treatment targets the underlying cause and the resulting dysfunction. In liver fibrosis, removing the source of injury (antiviral therapy, abstinence from alcohol, control of metabolic risk factors) can halt progression and, in some cases, promote regression. In pulmonary fibrosis, antifibrotic drugs such as pirfenidone and nintedanib can slow decline in many patients; advanced disease may require transplantation. Supportive care and management of complications are essential across organ systems.