Fibrosis

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Fibrosis
Cardiac amyloidosis very high mag movat.jpg
Micrograph of a heart showing fibrosis (yellow - left of image) and amyloid deposition (brown - right of image). Movat's stain.
Classification and external resources
Specialty Pathology
MeSH D005355

Fibrosis is the formation of excess fibrous connective tissue in an organ or tissue in a reparative or reactive process.[1] This can be a reactive, benign, or pathological state. In response to injury, this is called scarring, and if fibrosis arises from a single cell line, this is called a fibroma. Physiologically, fibrosis acts to deposit connective tissue, which can obliterate the architecture and function of the underlying organ or tissue. Fibrosis can be used to describe the pathological state of excess deposition of fibrous tissue, as well as the process of connective tissue deposition in healing.[2]

Physiology[edit]

Fibrosis is similar to the process of scarring, in that both involve stimulated fibroblasts laying down connective tissue, including collagen and glycosaminoglycans. The process is initiated when immune cells such as macrophages release soluble factors that stimulate fibroblasts. The most well characterized pro-fibrotic mediator is TGF beta, which is released by macrophages as well as any damaged tissue between surfaces called interstitium. Other soluble mediators of fibrosis include CTGF, platelet-derived growth factor (PDGF), and Interleukin 4 (IL-4). These initiate signal transduction pathways such as the AKT/mTOR[3] and SMAD[4] pathways that ultimately lead to the proliferation and activation of fibroblasts, which deposit extracellular matrix into the surrounding connective tissue.

Examples of fibrosis[edit]

Fibrosis can occur in many tissues within the body, typically as a result of inflammation or damage, and examples include:

Micrograph showing cirrhosis of the liver. The tissue in this example is stained with a trichrome stain, in which fibrosis is colored blue. The red areas are the nodular liver tissue

Lungs

Liver

Heart

Brain

Other

References[edit]

  1. ^ Birbrair, Alexander; Zhang, Tan; Files, Daniel C.; Mannava, Sandeep; Smith, Thomas; Wang, Zhong-Min; Messi, Maria L.; Mintz, Akiva; Delbono, Osvaldo (2014-11-06). "Type-1 pericytes accumulate after tissue injury and produce collagen in an organ-dependent manner". Stem Cell Research & Therapy 5 (6): 122. doi:10.1186/scrt512. ISSN 1757-6512. PMC 4445991. PMID 25376879. 
  2. ^ Glossary of dermatopathological terms. DermNet NZ
  3. ^ Mitra A, Luna JI, Marusina AI, Merleev A, Kundu-Raychaudhuri S, Fiorentino D, Raychaudhuri SP, Maverakis E (2015). "Dual mTOR Inhibition Is Required to Prevent TGF-β-Mediated Fibrosis: Implications for Scleroderma.". J Invest Dermatol 135 (11): 2873–6. doi:10.1038/jid.2015.252. PMID 26134944. 
  4. ^ Leask A, Abraham DJ (2004). "TGF-beta signaling and the fibrotic response". FASEB JOURNAL 18 (7): 816–827. doi:10.1096/fj.03-1273rev. PMID 15117886. 

External links[edit]