Abstract
Atherosclerosis is a leading cause of mortality and morbidity in the western world. It is no longer a disease attributed mainly to the high lipid content of the body but has come to be regarded as a chronic inflammatory disease with an autoimmune component. Studies which explore the interactions between molecular and cellular elements generally focus on pathophysiologic aspect of atherosclerosis. The focus has now shifted to the novel risk factors and the genetic predisposition which has further broadened the pathogenetic mechanisms. Hence, It's high time to understand these processes in depth so that new markers and treatments which target mechanisms specially inflammation which is now the most exact cause of atherosclerosis. Moreover, the diagnosis and management is the guiding element in the understanding, progression of chronic diseases like atherosclerosis. Therefore, targeting and understanding of biochemical pathways would help in more accurate diagnosis and management of disease. Additionally, the use of antihyperlipidemic and anti-inflammatory drugs for the treatment of atherosclerosis was only possibility but it had average results. Henceforth, delving into newer areas or novel drug targets like endoglin receptor, PPARα, squalene synthase, thyroid hormone analogues, scavenger receptors, Leucotriene receptors, calcium signaling, Pentraxin, nitric oxide, heat shock proteins, Liver X Receptors, shear stress pathway, CD14, endotoxin signaling, and nuclear factor kappa B give better treatment possibilities to control the process of atherosclerosis. Therefore, the review briefly focuses on molecular mechanisms involved in the evolution of the atherosclerotic plaque and different novel targets that act at the starting stage of the plaque form to the thrombus formation in the atherosclerosis that may pave the way for selecting optimal therapies and preventing plaque complications.
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