Fibrosis
Fibrosis is excessive connective tissue deposition disrupting organ function.
Wikipedia / Wikimedia Commons
Fibrosis, or fibrotic scarring, is the formation of fibrous connective tissue after an injury. This process can represent normal tissue repair or, in disease, excessive deposition that creates a permanent scar, potentially disrupting or blocking the normal structure and function of the affected organ or tissue.
Repeated injuries, chronic inflammation, and ongoing repair make fibrosis more likely. In these cases, fibroblasts overproduce extracellular matrix components, especially collagen, leading to a lasting fibrotic scar. When this occurs in response to injury, it is called scarring; if it arises from a single cell line, it is termed a fibroma. Physiologically, fibrosis deposits connective tissue, which can interfere with or completely inhibit normal organ architecture and function. The term describes both the pathological state of excess fibrous tissue and the connective tissue deposition process in healing. Defined by the abnormal accumulation of extracellular matrix (ECM) proteins, fibrosis results in scarring and thickening of affected tissue—essentially a natural wound healing response that disrupts normal organ function.
**Physiology** Fibrosis resembles scarring: both involve stimulated fibroblasts laying down connective tissue, including collagen and glycosaminoglycans. The process begins when immune cells like macrophages release soluble factors that activate fibroblasts. The best-known pro-fibrotic mediator is TGF beta, released by macrophages and any damaged interstitial tissue. Other soluble mediators include CTGF, platelet-derived growth factor (PDGF), and interleukin 10 (IL-10). These trigger signal pathways such as AKT/mTOR and SMAD, leading to fibroblast proliferation and activation, which deposit ECM into surrounding connective tissue. This tissue repair is complex, with tight regulation of ECM synthesis and degradation to maintain normal architecture. However, if injury is severe or repetitive, or if the wound healing response becomes unregulated, the process can lead to progressive, irreversible fibrosis.
**Anatomical location** Fibrosis can occur in many tissues, typically due to inflammation or damage.
Quick Facts
- Field
- Pathology, rheumatology
- Complications
- Cirrhosis
- Risks
- Repeated injuries, chronic inflammation.
Facts from the source article.
Lore & Background
Fibrosis is initiated when immune cells such as macrophages release soluble factors that stimulate fibroblasts. The most well characterized pro-fibrotic mediator is TGF beta, released by macrophages and damaged interstitium. Other mediators include CTGF, platelet-derived growth factor (PDGF), and interleukin 10 (IL-10), which initiate signal transduction pathways such as AKT/mTOR and SMAD pathways, leading to fibroblast proliferation and extracellular matrix deposition.
Reader's Guide
Fibrosis represents a natural wound healing response that can become pathological when tissue injury is severe or repetitive, or when the wound healing response becomes deregulated. It can occur in many tissues, including the lungs (pulmonary fibrosis, cystic fibrosis), liver (bridging fibrosis, cirrhosis), kidneys, brain (glial scar), and heart (myocardial fibrosis). Historically considered irreversible, recent studies have demonstrated reversal in liver and lung tissue, and in cases of renal, myocardial, and oral-submucosal fibrosis. The process involves tight regulation of extracellular matrix synthesis and degradation, but when disrupted, leads to progressive irreversible fibrotic scarring that interferes with normal organ function.
Did You Know?
- Fibrosis can be described as the pathological state of excess deposition of fibrous tissue, as well as the process of connective tissue deposition in healing.
- Senescence of hepatic stellate cells could prevent progression of liver fibrosis, though not yet implemented as therapy due to risks.
- Historically considered irreversible, fibrosis reversal has been demonstrated in liver, lung, renal, myocardial, and oral-submucosal tissues.
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