The molecular concept of atheromatous plaques

• Published in: Current Drug Targets
• Main Author: Thent Z.C.; Chakraborty C.; Mahakkanukrauh P.; Mahmood N.R.K.N.; Rajan R.; Das S.
• Format: Review
• Language: English
• Published: Bentham Science Publishers B.V. 2017
• Online Access: https://www.scopus.com/inward/record.uri?eid=2-s2.0-85028991757&doi=10.2174%2f1389450117666160502151600&partnerID=40&md5=679f3dfc496723bdd584bfb028225fa1

Background: Recently, there are scientific attempts to discover new drugs in the biotechnology industry in order to treat various diseases including atherosclerosis. Objective: The main objective of the present review was to highlight the cellular, molecular biology and inflammatory process related to the atheromatous plaques. Methods: A thorough literature search of Pubmed, Google and Scopus databases was done. Results: Atherosclerosis is considered to be a leading cause of death throughout the world. Atherosclerosis involves oxidative damage to the cells with production of reactive oxygen species (ROS). Development of atheromatous plaques in the arterial wall is a common feature. Specific inflammatory markers pertaining to the arterial wall in atherosclerosis may be useful for both diagnosis and treatment. These include Nitric oxide (NO), cytokines, macrophage inhibiting factor (MIF), leucocytes and Pselectin. Modern therapeutic paradigms involving endothelial progenitor cells therapy, angiotensin II type-2 (AT2R) and ATP-activated purinergic receptor therapy are notable to mention. Conclusion: Future drugs may be designed aiming three signalling mechanisms of AT2R which are (a) activation of protein phosphatases resulting in protein dephosphorylation (b) activation of bradykinin/nitric oxide/cyclic guanosine 3',5'-monophosphate pathway by vasodilation and (c) stimulation of phospholipase A(2) and release of arachidonic acid. Drugs may also be designed to act on ATP-activated purinergic receptor channel type P2X7 molecules which acts on cardiovascular system. © 2017 Bentham Science Publishers.