Please use this identifier to cite or link to this item: http://cmuir.cmu.ac.th/jspui/handle/6653943832/56840
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dc.contributor.authorZar Chi Thenten_US
dc.contributor.authorChiranjib Chakrabortyen_US
dc.contributor.authorPasuk Mahakkanukrauhen_US
dc.contributor.authorNik Ritza Kosai Nik Mahmooden_US
dc.contributor.authorReynu Rajanen_US
dc.contributor.authorSrijit Dasen_US
dc.date.accessioned2018-09-05T03:30:58Z-
dc.date.available2018-09-05T03:30:58Z-
dc.date.issued2017-01-01en_US
dc.identifier.issn18735592en_US
dc.identifier.issn13894501en_US
dc.identifier.other2-s2.0-85028991757en_US
dc.identifier.other10.2174/1389450117666160502151600en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85028991757&origin=inwarden_US
dc.identifier.urihttp://cmuir.cmu.ac.th/jspui/handle/6653943832/56840-
dc.description.abstract© 2017 Bentham Science Publishers. 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.en_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.subjectPharmacology, Toxicology and Pharmaceuticsen_US
dc.titleThe molecular concept of atheromatous plaquesen_US
dc.typeJournalen_US
article.title.sourcetitleCurrent Drug Targetsen_US
article.volume18en_US
article.stream.affiliationsUniversiti Teknologi MARAen_US
article.stream.affiliationsGalgotias Universityen_US
article.stream.affiliationsChiang Mai Universityen_US
article.stream.affiliationsUniversiti Kebangsaan Malaysiaen_US
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