Metabolic responses of extracellular matrix in tissue repair.
Tissue repair is a property of all vascularized tissues. A complex yet co-ordinated series of molecular and cellular events regulates repair, including its fibrogenic component that eventuates in fibrous tissue formation. This report suggests that phenotypically transformed fibroblast-like cells, termed myofibroblasts (myoFb) because they express alpha-smooth muscle actin, are responsible for collagen turnover at sites of repair. They impart extracellular matrix with metabolic and contractile activity. De novo generation of angiotensin II by myoFb at sites of repair has important autocrine and paracrine functions. Regressive, persistent and progressive forms of fibrosis are related to the fate of myoFb and the signals they generate.
Weber
K T
KT
Department of Internal Medicine, University of Missouri Health Sciences Center, Columbia, MO 65212, USA. medparky@showme.missouri.edu
D000808:Angiotensinogen / Q000378:metabolism; D000818:Animals; D017209:Apoptosis; D003094:Collagen / Q000096:biosynthesis; D005109:Extracellular Matrix / Q000378:metabolism*; D005347:Fibroblasts / Q000502:physiology; D005355:Fibrosis / Q000378:metabolism; D006801:Humans; D007703:Peptidyl-Dipeptidase A / Q000502:physiology; D012333:RNA, Messenger / Q000378:metabolism; D014945:Wound Healing / Q000502:physiology*
D012333:RNA, Messenger; D000808:Angiotensinogen; D003094:Collagen; D007703:Peptidyl-Dipeptidase A