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