Apoptosis or programmed cell death (PCD) is essential for the normal functioning and survival of most cells including those in the peripheral nervous system (PNS). The morphological appearance of apoptosis, the severity of cell death, and the mechanism of cell death might vary between different cell types in the PNS and between different mammalian models of diabetes. However, most cells show evidence of mitochondrial (Mt)

From: Contemporary Diabetes: Diabetic Neuropathy: Clinical Management, Second Edition Edited by: A. Veves and R. Malik © Humana Press Inc., Totowa, NJ

damage and some, if not all, the features of the original morphological descriptions of apoptosis (1-3). PCD has mainly been described in cell culture and animal models of diabetes, although there is also morphological evidence of apoptosis in Schwann cells (SC) from human sural nerve. Reactive oxygen species and the resulting oxidative stress play a pivotal role in apoptosis and are likely to primarily mediate their effect by causing dysregulation of Mt function. During Mt dysfunction, several essential players of apoptosis, including procaspases and cytochrome-c are released into the cytosol and result in the formation of multimeric complexes that induce apoptotic cell death. Antioxidants and certain regulators of the inner Mt membrane potential, for example, BCL proteins, uncoupling proteins (UCPs), and growth factors might prevent apoptosis in the PNS. Despite disagreements over the nature of apoptosis in some cells in the PNS, the actual importance of apoptosis in the PNS rests mainly in the pathways leading to apoptosis, and how intervention in these pathways might result in a reduction in the severity of peripheral neuropathy. This review will describe the pathological changes that distinguish apoptosis from other forms of cell death, describe known mechanisms of PCD, and finally discuss both evidence of PCD and mechanisms of PCD in the PNS.

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