Common and unique mechanisms regulate fibrosis in various fibroproliferative diseases.
Fibroproliferative diseases, including the pulmonary fibroses, systemic sclerosis, liver cirrhosis, cardiovascular disease, progressive kidney disease, and macular degeneration, are a leading cause of morbidity and mortality and can affect all tissues and organ systems. Fibrotic tissue remodeling can also influence cancer metastasis and accelerate chronic graft rejection in transplant recipients. Nevertheless, despite its enormous impact on human health, there are currently no approved treatments that directly target the mechanism(s) of fibrosis. The primary goals of this Review series on fibrotic diseases are to discuss some of the major fibroproliferative diseases and to identify the common and unique mechanisms of fibrogenesis that might be exploited in the development of effective antifibrotic therapies.
Wynn
Thomas A
TA
Immunopathogenesis Section, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892, USA. twynn@niaid.nih.gov
D000804:Angiotensin II / Q000502:physiology; D049109:Cell Proliferation; D002908:Chronic Disease; D053595:Embryonic Stem Cells / Q000637:transplantation; D005347:Fibroblasts / Q000473:pathology / Q000502:physiology*; D005355:Fibrosis / Q000209:etiology* / Q000276:immunology / Q000628:therapy; D006801:Humans; D007239:Infections / Q000276:immunology; D009389:Neovascularization, Pathologic / Q000276:immunology / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000502:physiology; D014945:Wound Healing
D053773:Transforming Growth Factor beta1; D000804:Angiotensin II