Abstract
Apoptosis plays an important role in organ development and repair, however, it is becoming clear that it may also be involved in a number of different diseases. In recent years, there has been growing evidence to implicate apoptosis in kidney development [1, 2] and various renal disorders including immune-mediated renal disease, polycystic kidney disease and acute tubular necrosis. Many of the proteins involved in the apoptotic mechanism are present in the kidney and their expression and/or activity are altered under different conditions and are associated with changes in structure and function. For example, the Fas receptor, which when stimulated by Fas, induces apoptosis [3, 4] is expressed in a number of renal cells including mesangial cells [5] and tubular epithelial cells [6]. Furthermore, renal Fas expression increases in rats following induction of endotoxemia and this is accompanied by evidence of apoptosis along the nephron [5]. Other important mediators of apoptosis are a novel family of cysteine proteases, termed caspases [7], and there is recent evidence indicating that there is an altered expression of members of this family in the rat kidney following ischemia reperfusion injury [8].
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Wong, V.Y., Ali, S.M., Brooks, D.P. (1999). Apoptosis in renal disease. In: Winkler, J.D. (eds) Apoptosis and Inflammation. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8741-0_13
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DOI: https://doi.org/10.1007/978-3-0348-8741-0_13
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