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Published in

Bentham Science Publishers, Current Protein & Peptide Science, 3(22), p. 228-236, 2021

DOI: 10.2174/1389203721999201208200242

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Understanding the role of Inflammasome in Angina Pectoris

This paper was not found in any repository, but could be made available legally by the author.
This paper was not found in any repository, but could be made available legally by the author.

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Abstract

Angina pectoris, associated with coronary artery disease, a cardiovascular disease where the pain is caused by adverse oxygen supply in the myocardium, results in contractility and discomfort in the chest. Inflammasomes, triggered by stimuli due to infection and cellular stress, have been identified to play a vital role in the progression of cardiovascular disorders and, thus, causing various symptoms like angina pectoris. Nlrp3 inflammasome, a key contributor in the pathogenesis of angina pectoris, requires activation and primary signaling for the commencement of inflammation. Nlrp3 inflammasome elicits out an inflammatory response by the emission of pro-inflammatory cytokines by ROS (reactive oxygen species) production, mobilization of K<sup>+</sup> efflux and Ca<sup>2+</sup> and by activation of lysosome destabilization that eventually causes pyroptosis, a programmed cell death process. Thus, inflammasome is considered to be one of the factors involved in the progression of coronary artery diseases and has an intricate role in the development of angina pectoris.