摘要 : Context: Atherosclerosis is a progressive pathological process and a leading cause ofmortality worldwide. Clinical research and epidemiological studies state that atherosclerosis iscaused by an amalgamation of metabolic and inflam... 展开 Context: Atherosclerosis is a progressive pathological process and a leading cause ofmortality worldwide. Clinical research and epidemiological studies state that atherosclerosis iscaused by an amalgamation of metabolic and inflammatory deregulation involving three importantpathological events including Endothelial Dysfunction (ED), Foam Cell Formation (FCF), andVascular Smooth Muscle Cells (VSMCs) proliferation and migration.Objectives: Research in recent years has identified Metabolic Syndrome (MS), which involves factorssuch as obesity, insulin resistance, dyslipidemia and diabetes, to be responsible for the pathophysiologyof atherosclerosis. These factors elevate oxidative stress and inflammation-induced keysignalling molecules and various microRNAs (miRs). In present study, we have reviewed recentlyidentified molecular targets in the pathophysiology of atherosclerosis.Methods: Scientific literature obtained from databases such as university library, PubMed andGoogle along with evidences from published experimental work in relevant journals has beensummarized in this review article.Results: The molecular events and cell signalling implicated in atherogenic processes of ED, FCFand VSMCs hyperplasia are sequential and progressive, and involve cross talks at many levels.Specific molecules such as transcription factors, inflammatory cytokines and chemokines and miRshave been identified playing crucial role in most of the events leading to atherosclerosis.Conclusion: Studies associated with MS induced oxidative stress- and inflammation- mediatedsignalling pathways along with critical miRs help in better understanding of the pathophysiology ofatherosclerosis. Several key molecules discussed in this review could be potent target for the preventionand treatment of atherosclerosis. 收起