Role of Caveolin-1 in Inflammation: Genetic Predisposition and Potential Implication for Multiple Sclerosis

Multiple Sclerosis (MS), a chronic, immune-mediated disease of the central nervous system (CNS) is typified by leukocyte infiltration into CNS, inflammation, demyelination, and neurodegeneration. Risk factors include genetic predispositions involving HLA-DR15 and various single nucleotide polymorphisms affecting T cell function. Early signs such as blurred/double vision, numbness, fatigue, and balance coordination, are later accompanied by cognitive as well as bladder and bowel dysfunction. Genetic models of neuroinflammation have helped development of drugs with significant effects on progression and relapse rate of MS. Nonetheless, MS continues to pose major challenges as the pathological mechanisms remain unclear. Recent studies highlight the crucial role of quality and organization of cytoskeletal proteins in maintaining complex cellular functions such as neuronal excitability and neuroinflammation. Understanding how changes in these proteins impact demyelination is key to drug development for MS. Systems biology, an interdisciplinary field of study posits that complex interactions within biological systems contribute to the inflammatory processes and suggests that Cav-1, an integral membrane protein of caveolae with crucial role in cell signaling may provide a novel target in MS. Herein, we examine potential genetic influences on Cav-1 and its role in inflammation and demyelination in relation to MS. Specifically, its roles in oxidative stress, inflammation, blood brain barrier (BBB) integrity, and autophagy are discussed. Nonetheless, we conclude that translational aspect of Cav-1 and hence its specific therapeutic targeting in MS requires further exploration.