Inflammatory basis of atherosclerosis: Modulation by sex hormones
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Bentham Science Publishers
Abstract
Atherosclerosis-related cardiovascular diseases (CVDs) are the leading cause of death globally. Several lines of evidence are supportive of the contributory role of vascular inflammation in atherosclerosis. Di-verse immune cell types, including monocytes/macrophages, T-cells and neutrophils, as well as specialized pro-resolving lipid mediators, have been successfully characterized as key players in vascular inflammation. The increased prevalence of atherosclerotic CVD in men in comparison to age-matched premenopausal women and the abolition of sex differences in prevalence during menopause strongly suggest a pivotal role of sex hormones in the development of CVD. Indeed, many animal and human studies conclusively implicate sex hormones as a crucial component in driving the immune response. This is further corroborated by the effective identification of sex hormone receptors in vascular endothelial cells, vascular smooth muscle cells and immune cells. Collectively, these findings suggest a cellular communication between sex hormones and vascular or immune cells underlying the vascular inflammation in atherosclerosis. The aim of this review is to provide an overview of vascular inflammation as a causal cue underlying atherosclerotic CVDs within the context of the modulatory effects of sex hormones. Moreover, the cellular and molecular signaling pathways underlying the sex hormones-immune system interactions as potential culprits for vascular inflammation are highlighted with detailed and critical discussion. Finally, the review concludes by speculations on the potential sex-related efficacy of currently available immunotherapies in mitigating vascular inflammation. Conceivably, a deeper understanding of the immunoregulatory influence of sex hormones on vascular inflammation-mediated atherosclerosis permits sex-based management of atherosclerosis-related CVDs. © 2021 Bentham Science Publishers.
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Adhesion molecules, Atherosclerosis, Cytokines, Estrogen, Immune cells, Inflammasome, Testosterone, Animals, Endothelial cells, Female, Gonadal steroid hormones, Humans, Inflammation, Male, Sex characteristics, Signal transduction, Androgen receptor, C reactive protein, Cd36 antigen, Cell adhesion molecule, Cyclooxygenase 2, Cytokine, Endothelial leukocyte adhesion molecule 1, Estrogen receptor, Fractalkine, G protein coupled receptor, G protein coupled receptor 30, Gamma interferon, Hormone receptor, Immunoglobulin enhancer binding protein, Intercellular adhesion molecule 1, Interleukin 1, Interleukin 10, Interleukin 12, Interleukin 13, Interleukin 17, Interleukin 18, Interleukin 1beta, Interleukin 23, Interleukin 4, Interleukin 6, Low density lipoprotein, Mitogen activated protein kinase, Monocyte chemotactic protein 1, Oxidized low density lipoprotein, Progesterone receptor, Reactive oxygen metabolite, Scavenger receptor bi, Sex hormone, Sirtuin 1, Stat3 protein, Stress activated protein kinase, Transcription factor nrf2, Tumor necrosis factor, Vascular cell adhesion molecule 1, Antigen presenting cell, Aortic intima, Autoimmune disease, Breast cancer, Cardiovascular disease, Cd4+ t lymphocyte, Cd8+ t lymphocyte, Cholinergic nerve cell, Cytokine production, Down regulation, Endoplasmic reticulum, Extracellular trap, Gene overexpression, Human, Huvec cell line, Immune response, Immune system, Immunocompetent cell, Immunomodulation, Immunoregulation, Immunotherapy, M2 macrophage, Macrophage, Multiple sclerosis, Neutrophil, Nf kb signaling, Psoriasis, Review, Systemic lupus erythematosus, T lymphocyte, Th17 cell, Vasculitis, Vasodilatation, Animal, Endothelium cell, Sexual characteristics