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      Growth factors and apoptosis in acute renal injury.

      Current Opinion in Nephrology and Hypertension
      Acute Kidney Injury, genetics, physiopathology, Animals, Apoptosis, drug effects, physiology, Growth Substances, pharmacology, Humans, Kidney, pathology, Proto-Oncogenes

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          The precisely orchestrated pattern of growth factor expression within the kidney following acute renal injury indicates that growth factors regulate the process of repair. The use of growth factors as therapeutic agents to accelerate renal regeneration in this setting stems from this observation. In animal models of acute renal injury, administration of epidermal growth factor (EGF), insulin-like growth factor I (IGF-I) or hepatocyte growth factor (HGF) accelerates restoration of kidney function and normalization of histology post-acute renal injury and reduces mortality. IGF-I has been safely administered to humans and protects against post-surgical renal dysfunction. Renal cellular apoptosis occurs in a predictable pattern during recovery from acute ischemic injury. Renal apoptosis is regulated by agents both intrinsic and extrinsic to the kidney cell. The protooncogene, B-cell lymphoma/leukemia gene product-2 (bcl-2), is an important intrinsic factor. The growth factor, EGF, is an important extrinsic regulator. A thorough understanding of the control of renal apoptosis during recovery from ischemic injury coupled with an increased understanding of the roles that growth factors play in this process, is likely to result in the development of new therapies to enhance kidney regeneration.

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          Acute Kidney Injury,genetics,physiopathology,Animals,Apoptosis,drug effects,physiology,Growth Substances,pharmacology,Humans,Kidney,pathology,Proto-Oncogenes


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