This review will seek to further extend such LR redox signaling concept to different areas as a common signaling mechanism and thoroughly introduce the latest advances in its molecular mechanisms and the corresponding physiological and pathological relevance. Major advances in LR redox signaling in specific cell types have been reported and reviewed by a series of excellent papers that have added much to the literature ( 192, 235, 283, 446). Many studies have shown that LRs or their platforms can participate in the signaling of cell apoptosis or dysfunction associated with oxidative stress during activation of various death receptors ( 385). Recently collected evidence suggests that membrane lipid rafts (LRs) and their platforms may represent an important mechanism by which redox signals are produced and transmitted in response to various agonists or stimuli ( 234, 283, 423, 446). Redox injury, as a pathological mechanism, is also involved in a wide range of pathophysiological processes such as senescence ( 65), inflammation ( 17, 264, 421), hypoxia ( 32, 148, 200, 245), and ischemia/reperfusion ( 126, 379, 384), which contribute to the progression of almost all diseases, from cardiovascular ones such as shock ( 94, 116, 117), hypertension ( 73, 167, 288, 294, 316, 440), atherosclerosis ( 208, 297), to metabolic ones such as diabetes mellitus ( 20, 217), neurodegenerative ones such as Alzheimer's disease (AD) ( 55, 305), infectious diseases ( 184, 252, 285, 375), and cancer ( 16, 292, 409).ĭespite extensive research, the exact mechanism by which redox enzymes are promptly activated by different stimuli still remains poorly understood, perhaps because enzymes such as NADPH oxidase, unlike G-protein-coupled enzymes, are not linked directly with any specific receptors. R edox signaling is increasingly regarded as an important cellular process in a variety of cellular activities, including cell proliferation ( 50, 52, 275), differentiation ( 72, 153, 219, 337, 338), and apoptosis ( 162, 242, 254, 304, 413). It is hoped that all information and thoughts included in this review could provide more comprehensive insights into the understanding of lipid raft redox signaling, in particular, of their molecular mechanisms, spatial-temporal regulations, and physiological, pathophysiological relevances to human health and diseases. Several molecular mechanisms involving the formation of lipid raft redox signaling platforms and the related therapeutic strategies targeting them are discussed. This comprehensive review attempts to summarize all basic and advanced information about the formation, regulation, and functions of lipid raft redox signaling platforms as well as their physiological and pathophysiological relevance. In particular, this raft platform formation provides an important driving force for the assembling of NADPH oxidase subunits and the recruitment of other related receptors, effectors, and regulatory components, resulting, in turn, in the activation of NADPH oxidase and downstream redox regulation of cell functions. Lipid rafts, the sphingolipid and cholesterol-enriched membrane microdomains, are able to form different membrane macrodomains or platforms upon stimulations, including redox signaling platforms, which serve as a critical signaling mechanism to mediate or regulate cellular activities or functions.
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