Neuronal and Schwann Cell Death in Diabetic Neuropathy

摘要: The balance of evidence supports the concept that programmed cell death (PCD) occurs in cells peripheral nervous system (PNS) presence diabetes, elevated glucose levels, or insulin deprivation. morphological appearance apoptosis, severity death, and mechanism might vary between different types PNS mammalian models diabetes. However, most show mitochondrial (Mt) damage some, if not all, features original descriptions apoptosis. PCD has mainly been described culture animal although there is also apoptosis Schwann from human sural nerve. Evidence organellar often exceeds observed dorsal root ganglion neuronal loss. Apoptosis represents only final pathological observation this state failure suboptimal organelle function. It likely even nonapoptotic neurons exhibit impaired metabolic function protein synthesis dysregulation will part induce neuropathy. One potential for induction diabetes-induced generation reactive oxygen species Mt During dysfunction, several essential players including procaspases cytochrome-c are released into cytosol result formation multimeric complexes apoptotic death. Antioxidants certain regulators inner membrane potential, example B-cell lymphoma (BCL) proteins, uncoupling growth factors prevent PNS. primary precipitating events leading to need be clearly delineated it understood how intervene common complication namely