Affiliations 

  • 1 Anatomy Unit, Faculty of Medicine, Universiti Teknologi MARA (UiTM), Sungai Buloh Campus, Jalan Hospital, 47000 Sungai Buloh, Selangor. Malaysia
  • 2 Department of Bioinformatics, School of Computer and Information Sciences, Galgotias, University, Uttar Pradesh. India
  • 3 Forensic Osteology Research Center, Excellence in Osteology Research and Training Center (ORTC) & Department of Anatomy, Chiang Mai University, Chiang Mai. Thailand
  • 4 Department of Surgery, Faculty of Medicine, Universiti Kebangsaan Malaysia 56000, Kuala Lumpur. Malaysia
  • 5 Department of Anatomy, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Jalan Yaacob Latif, Bandar Tun Razak 56000, Kuala Lumpur. Malaysia
Curr Drug Targets, 2017;18(11):1250-1258.
PMID: 27138760 DOI: 10.2174/1389450117666160502151600

Abstract

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 (AT<sub>2</sub>R) and ATP-activated purinergic receptor therapy are notable to mention.

CONCLUSION: Future drugs may be designed aiming three signalling mechanisms of AT<sub>2</sub>R which are (a) activation of protein phosphatases resulting in protein dephosphorylation (b) activation of bradykinin/nitric oxide/cyclic guanosine 3&#039;,5&#039;-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.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.