A disease condition where changes in extracellular matrix fibers occur, potentially diagnosable via polarized light.Fibrosis is the excessive accumulation of scar tissue in an organ. When tissue is injured, the normal repair process lays down a temporary scaffold of collagen and other extracellular matrix proteins, then removes it once healing is complete. In fibrosis, that removal never happens. The matrix keeps being produced, the scar grows, and the functional tissue it replaces is lost. Because the matrix is stiff and poorly supplied with blood, the organ gradually loses its ability to do its job — the lung cannot exchange oxygen, the liver cannot filter blood, the kidney cannot clean it.
Fibrosis is not a single disease but a final common pathway that can be triggered by many insults: chronic infection, alcohol, autoimmune attack, radiation, or persistent inflammation. It can affect almost any organ, and in the lung, liver, kidney and heart it is a major cause of disability and death. The condition is often diagnosed by imaging and biopsy, and the extracellular matrix changes can be visualised under a microscope using polarised light, because organised collagen fibres rotate the plane of polarised light and appear bright against a dark background.
The central cellular actor is the myofibroblast, a specialised cell that produces large amounts of collagen and contracts the scar. In normal wound healing myofibroblasts disappear once the wound closes; in fibrosis they persist and multiply, driven by signals such as TGF-beta. Because the process is self-sustaining, fibrosis tends to progress even if the original injury is removed.
The term fibrosis (from Latin fibra, fibre) came into medical use in the nineteenth century to describe the hardened, fibrous appearance of diseased organs at autopsy; the central role of the myofibroblast was established in the 1970s by Gabbiani and colleagues.
The mechanism begins with injury to epithelial or endothelial cells, which release inflammatory mediators and recruit immune cells. These cells, in turn, secrete cytokines — especially TGF-beta and PDGF — that activate resident fibroblasts and other precursor cells. The activated cells transform into myofibroblasts, which synthesise collagen types I and III, fibronectin and other matrix components at a high rate.
At the same time, the enzymes that normally degrade matrix, the matrix metalloproteinases, are inhibited by tissue inhibitors of metalloproteinases, so the balance shifts decisively toward accumulation. The stiffening matrix itself sends mechanical signals back to the cells, reinforcing the myofibroblast state in a positive feedback loop. The result is a dense, cross-linked scar that is resistant to breakdown and disrupts the architecture of the surrounding tissue.
Antifibrotic drugs such as pirfenidone and nintedanib are used to slow the progression of idiopathic pulmonary fibrosis, and research continues into therapies that target TGF-beta signalling or the myofibroblast itself.
Polarised light microscopy of a fibrotic tissue section can make collagen fibres glow brightly against a dark background, because the aligned protein fibres rotate the plane of polarised light — a property called birefringence.