Hamideh Kouhpeikar1, Zahra Delbari2, Thozhukat Sathyapalan3, Luis E Simental-Mendía4, Tannaz Jamialahmadi5,6, Amirhossein Sahebkar7,8,9. 1. Department of hematology and blood bank, Tabas school of nursing, Birjand University of Medical Science, Birjand, Iran. 2. Inflammation and Inflammatory Diseases Research Center, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. 3. Department of Academic Diabetes, Endocrinology and Metabolism, Hull York Medical School, University of Hull, Hull, HU3 2JZ, UK. 4. Biomedical Research Unit, Mexican Social Security Institute, Durango, Mexico. 5. Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran. 6. Department of Nutrition, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. 7. Halal Research Center of IRI, FDA, Tehran, Iran. sahebkara@mums.ac.ir. 8. Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. sahebkara@mums.ac.ir. 9. School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran. sahebkara@mums.ac.ir.
Abstract
PURPOSE OF REVIEW: In this review, we discuss the evidence supporting the effects of statins on mast cells (MCs) in atherosclerosis and their molecular mechanism of action. RECENT FINDINGS: Statins or HMG-CoA reductase inhibitors are known for their lipid-lowering properties and are widely used in the prevention and treatment of cardiovascular diseases. There is growing evidence that statins have an inhibitory effect on MCs, which contributes to the pleiotropic effect of statins in various diseases. MCs are one of the crucial effectors of the immune system which play an essential role in the pathogenesis of multiple disorders. Recent studies have shown that MCs are involved in the development of atherosclerotic plaques. MCs secrete various inflammatory cytokines (IL-6, IL4, TNF-α, and IFNγ) and inflammatory mediators (histamine, tryptase, proteoglycans) after activation by various stimulants. This, in turn, will exacerbate atherosclerosis. Statins suppress the activation of MCs via IgE inhibition which leads to inhibition of inflammatory mediators and cytokines which are involved in the development and progression of atherosclerosis. In keeping with this evidence presented here, MCs can be considered as one of the therapeutic targets for statins in the treatment of atherosclerosis.
PURPOSE OF REVIEW: In this review, we discuss the evidence supporting the effects of statins on mast cells (MCs) in atherosclerosis and their molecular mechanism of action. RECENT FINDINGS: Statins or HMG-CoA reductase inhibitors are known for their lipid-lowering properties and are widely used in the prevention and treatment of cardiovascular diseases. There is growing evidence that statins have an inhibitory effect on MCs, which contributes to the pleiotropic effect of statins in various diseases. MCs are one of the crucial effectors of the immune system which play an essential role in the pathogenesis of multiple disorders. Recent studies have shown that MCs are involved in the development of atherosclerotic plaques. MCs secrete various inflammatory cytokines (IL-6, IL4, TNF-α, and IFNγ) and inflammatory mediators (histamine, tryptase, proteoglycans) after activation by various stimulants. This, in turn, will exacerbate atherosclerosis. Statins suppress the activation of MCs via IgE inhibition which leads to inhibition of inflammatory mediators and cytokines which are involved in the development and progression of atherosclerosis. In keeping with this evidence presented here, MCs can be considered as one of the therapeutic targets for statins in the treatment of atherosclerosis.
Authors: Amir Vahedian-Azimi; Sajad Shojaie; Maciej Banach; Farshad Heidari; Arrigo F G Cicero; Masoum Khoshfetrat; Tannaz Jamialahmadi; Amirhossein Sahebkar Journal: Ann Med Date: 2021-12 Impact factor: 4.709