Transforming growth factor-beta and angiotensin in fibrosis and burn injuries.
This review considers the roles of transforming growth factor-beta (TGF-beta), the signaling Smad proteins, and angiotensin II (AT II) in conditions leading to human fibrosis. The goal is to update the burn practitioner and researcher about this important pathway and to introduce AT II as a possible synergistic signal to TGF-beta in burn scarring. Literature searches of the MEDLINE database were performed for English manuscripts combinations of TGF-beta, Smad, angiotensin, fibrosis, burn, and scar. AT II and TGF-beta both activate the Smad protein system, which leads to the expression of genes related to fibrosis. In fibrotic conditions, such as tubulointerstitial nephritis, systemic sclerosis, and myocardial infarctions, AT II acts both independently and synergistically with TGF-beta. Both AT II and TGF-beta act through a messenger system, the Smad proteins that lead to excessive extracellular matrix formation. Treatment and research implications are reviewed. The interaction between AT II and TGF-beta leading to fibrosis is well described in some human diseases. This pathway may be of importance in human burn scarring as well.
Gabriel
Vincent Ashley
VA
Department of Physical Medicine and Rehabilitation, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9055, USA.
D000809:Angiotensins / Q000378:metabolism*; D002056:Burns / Q000378:metabolism*; D005355:Fibrosis / Q000378:metabolism; D006801:Humans; D009203:Myocardial Infarction / Q000378:metabolism; D012594:Scleroderma, Localized / Q000378:metabolism; D015398:Signal Transduction; D051785:Smad Proteins / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000378:metabolism*
D000809:Angiotensins; D051785:Smad Proteins; D016212:Transforming Growth Factor beta