Abstract:
: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.
journal_name
Ren Failjournal_title
Renal failureauthors
Docherty NG,Pérez-Barriocanal F,Balboa NE,López-Novoa JMdoi
10.1081/jdi-120006767subject
Has Abstractpub_date
2002-07-01 00:00:00pages
391-406issue
4eissn
0886-022Xissn
1525-6049journal_volume
24pub_type
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