A Spotlight on the Underlying Activation Mechanisms of the NLRP3 Inflammasome and its Role in Atherosclerosis: A Review
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REVIEW
A Spotlight on the Underlying Activation Mechanisms of the NLRP3 Inflammasome and its Role in Atherosclerosis: A Review Anam Liaqat ,1,3 Muhammad Asad,2 Fatima Shoukat,1 and Arif-Ullah Khan1
Abstract— The world’s number one cause of death is cardiovascular diseases. The pathogenesis of different disease entities in the cardiovascular disease spectrum is complicated and multifactorial. Inflammation in these complicated etiologies serves as a key position and is a significant cause of atherosclerosis, which contributes to the underlying pathology. Therefore, therapeutic targeting of inflammatory pathways in patients with cardiovascular diseases such as atherosclerosis enhances cardiovascular results. Inflammasomes are intracellular protein complexes engaged in atherosclerosis pathogenesis and activated by multiple danger signals. Emerging proof has revealed that Nod-like receptor protein 3 (NLRP3) inflammasome, which regulates caspase-1 activation and later pro-interleukin processing, triggers inflammatory reactions in the vascular wall and leads to atherosclerotic plaque formation. Inflammasome-mediated signaling interference could decrease inflammation and mitigate illness severity. In this section, we provide an overview of the present literature on the underlying mechanisms leading to the activation of NLRP3 inflammasome and the role of NLRP3 inflammasome in the progression of atherogenesis and highlight the possibility of therapeutic interventions due to mechanisms involved in the of inhibition of NLRP3 activation. KEY WORDS: atherosclerosis; cardiovascular disease; inflammasome; inflammation; interleukin-1β.
a biochemical basis. Inflammasomes are protein structures that provide a platform for molecular signaling to activate caspase-1 and to regulate maturation of powerful proinflammatory cytokine interleukin-one beta, (IL-1 β) hence, contributing towards inflammatory cell death, in
INTRODUCTION Inflammation is the basis of a broad range of physiological and pathological processes. In particular, chronic inflammation for many modern human diseases constitutes Electronic Supplementary material The online version of this article (https://doi.org/10.1007/s10753-020-01290-1) contains supplementary material, which is available to authorized users. Highlights • Cardiovascular diseases involving heart and vasculature disorders are a serious global health burden that is presently the world’s leading cause of death. • Multiple danger signals such as cholesterol crystals, calcium phosphate crystals, and oxidized low-density lipoprotein triggered NLRP3 inflammasome activation in macrophages to initiate inflammatory reactions in atherosclerotic lesions.
• Understanding NLRP3 inflammasome activation mechanisms will allow its particular inhibitors to be developed to treat NLRP3-related illnesses 1
Riphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad, 44000, Pakistan 2 Armed Forces Institute of Cardiology, National Institute of Heart Diseases, Rawalpindi, Pakistan 3 To whom corre
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