Fibrotisation

Fibrotisation is the process by which normal tissue is progressively replaced with fibrous connective tissue, a form of fibrosis. It results from chronic injury, inflammation, or repeated wound healing and leads to stiffening and loss of function in the affected tissue.

In mechanism, activated fibroblasts and myofibroblasts synthesize excessive extracellular matrix, including collagen types I and III and fibronectin. Myofibroblasts can arise from resident fibroblasts, pericytes, or via transitions from epithelial or endothelial cells. Transforming growth factor-beta (TGF-β) is a key mediator, supported by other cytokines and oxidative stress. Excess matrix disrupts normal architecture and impairs tissue compliance and function.

Fibrotisation occurs in many organs, notably the liver (fibrosis and cirrhosis), lungs (pulmonary fibrosis), kidneys (interstitial fibrosis), heart (cardiac fibrosis), and skin (scleroderma). It can result from chronic infections, autoimmune diseases, toxins, metabolic disorders, or ischemic injury.

Diagnosis often relies on imaging and histology. MRI or CT can reveal architectural distortion and tissue heterogeneity; biopsy with staining for collagen confirms fibrosis. Non-invasive biomarkers and elastography help estimate fibrotic burden.

Treatment aims to limit ongoing injury and slow progression; there is no universal cure. Management includes addressing the underlying cause, anti-fibrotic therapies in select diseases, and supportive care. Research focuses on pathways such as TGF-β signaling, myofibroblast activity, and matrix remodeling, with the goal of preventing or reversing fibrotisation.