TrialLineage Concept
Fibrosis
Fibrosis is the formation of excess fibrous connective tissue in an organ, usually as a result of injury or chronic disease. It represents a failure of normal tissue repair — where the wound-healing process does not stop, leading to progressive scarring that impairs organ function.
What is fibrosis?
When tissue is injured, the body initiates a repair process. Fibroblasts migrate to the injury site and produce collagen and other extracellular matrix proteins to patch the damage. Normally, this process resolves once the wound is healed. In fibrotic diseases, the repair process becomes self-perpetuating — fibroblasts continue producing matrix proteins even after the original injury has resolved, gradually replacing functional tissue with dense scar tissue.
Fibrosis can affect virtually any organ: lungs (pulmonary fibrosis), liver (cirrhosis), kidneys (renal fibrosis), heart (cardiac fibrosis), and skin (scleroderma). Despite affecting different organs, fibrotic diseases share common cellular and molecular mechanisms centered on fibroblast activation and extracellular matrix accumulation.
Connection to the IPF lineage
Fibrosis is the central pathological process in idiopathic pulmonary fibrosis. The BMS-986278 trial tests whether blocking a specific profibrotic signaling pathway (LPA1) can slow the fibrotic process in the lung. Understanding fibrosis as a targetable biological mechanism — not just end-stage scarring — is what makes antifibrotic drug development possible.