Transforming growth factor-beta1 (TGF-beta1): a potential recovery signal in the post-ischemic kidney.
TGF-beta1 has been demonstrated to be up-regulated in response to ischemic events both in animal models and in man. Demonstration of this up-regulation in the kidney following experimentally induced acute renal failure and in renal transplants complements similar findings in coronary and cerebral ischemia. Activation of TGF-beta1 occurs as a direct consequence of hypoxia, angiotensin II signaling and loss of extra cellular matrix (ECM) integrity, all of which occur in renal ischemia-reperfusion injury. TGF-beta1 thus up-regulates the synthesis of extracellular matrix components such as fibronectin and collagen IV providing a basis for the restoration of epithelial coverage in the regenerating tubule. TGF-beta1 also regulates epithelial tubular cell proliferation and differentiation. This response is quickly closed down in response to recovery of the kidney. This review examines the evidence linking TGF-beta1 activity to recovery from renal ischemia thereby constructing a hypothesis for the beneficial role of TGF-beta1 in the post ischemic kidney.
Docherty
Neil G
NG
Instituto Reina Sofia de Investigación Nefrológia, Department of Physiology and Pharmacology, University of Salamanca, Spain.
Pérez-Barriocanal
Fernando
F
Balboa
Nelida E
NE
López-Novoa
José M
JM
D058186:Acute Kidney Injury / Q000503:physiopathology; D000804:Angiotensin II / Q000502:physiology; D000818:Animals; D006801:Humans; D007511:Ischemia / Q000503:physiopathology*; D007668:Kidney / Q000098:blood supply*; D015427:Reperfusion Injury / Q000503:physiopathology; D016212:Transforming Growth Factor beta / Q000378:metabolism / Q000502:physiology*; D015854:Up-Regulation / Q000502:physiology
D016212:Transforming Growth Factor beta; D000804:Angiotensin II