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      Increased thyroid stimulating hormone (TSH) as a possible risk factor for atherosclerosis in subclinical hypothyroidism

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          Abstract

          Primary hypothyroidism (PHT) is associated with an increased risk for the development of atherosclerosis (AS) and other cardiovascular disorders. PHT induces atherosclerosis (AS) through the induction of endothelial dysfunction, and insulin resistance (IR). PHT promotes vasoconstriction and the development of hypertension. However, patients with subclinical PHT with normal thyroid hormones (THs) are also at risk for cardiovascular complications. In subclinical PHT, increasing thyroid stimulating hormone (TSH) levels could be one of the causative factors intricate in the progression of cardiovascular complications including AS. Nevertheless, the mechanistic role of PHT in AS has not been fully clarified in relation to increased TSH. Therefore, in this review, we discuss the association between increased TSH and AS, and how increased TSH may be involved in the pathogenesis of AS. In addition, we also discuss how L-thyroxine treatment affects the development of AS.

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          The changing landscape of atherosclerosis

          Emerging evidence has spurred a considerable evolution of concepts relating to atherosclerosis, and has called into question many previous notions. Here I review this evidence, and discuss its implications for understanding of atherosclerosis. The risk of developing atherosclerosis is no longer concentrated in Western countries, and it is instead involved in the majority of deaths worldwide. Atherosclerosis now affects younger people, and more women and individuals from a diverse range of ethnic backgrounds, than was formerly the case. The risk factor profile has shifted as levels of low-density lipoprotein (LDL) cholesterol, blood pressure and smoking have decreased. Recent research has challenged the protective effects of high-density lipoprotein, and now focuses on triglyceride-rich lipoproteins in addition to low-density lipoprotein as causal in atherosclerosis. Non-traditional drivers of atherosclerosis-such as disturbed sleep, physical inactivity, the microbiome, air pollution and environmental stress-have also gained attention. Inflammatory pathways and leukocytes link traditional and emerging risk factors alike to the altered behaviour of arterial wall cells. Probing the pathogenesis of atherosclerosis has highlighted the role of the bone marrow: somatic mutations in stem cells can cause clonal haematopoiesis, which represents a previously unrecognized but common and potent age-related contributor to the risk of developing cardiovascular disease. Characterizations of the mechanisms that underpin thrombotic complications of atherosclerosis have evolved beyond the 'vulnerable plaque' concept. These advances in our understanding of the biology of atherosclerosis have opened avenues to therapeutic interventions that promise to improve the prevention and treatment of now-ubiquitous atherosclerotic diseases.
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            Immunity and Inflammation in Atherosclerosis.

            There is now overwhelming experimental and clinical evidence that atherosclerosis is a chronic inflammatory disease. Lessons from genome-wide association studies, advanced in vivo imaging techniques, transgenic lineage tracing mice, and clinical interventional studies have shown that both innate and adaptive immune mechanisms can accelerate or curb atherosclerosis. Here, we summarize and discuss the pathogenesis of atherosclerosis with a focus on adaptive immunity. We discuss some limitations of animal models and the need for models that are tailored to better translate to human atherosclerosis and ultimately progress in prevention and treatment.
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              Research Progress on the Relationship between Atherosclerosis and Inflammation

              Atherosclerosis is a chronic inflammatory disease; unstable atherosclerotic plaque rupture, vascular stenosis, or occlusion caused by platelet aggregation and thrombosis lead to acute cardiovascular disease. Atherosclerosis-related inflammation is mediated by proinflammatory cytokines, inflammatory signaling pathways, bioactive lipids, and adhesion molecules. This review discusses the effects of inflammation and the systemic inflammatory signaling pathway on atherosclerosis, the role of related signaling pathways in inflammation, the formation of atherosclerosis plaques, and the prospects of treating atherosclerosis by inhibiting inflammation.
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                Author and article information

                Contributors
                drmariospapadakis@gmail.com
                heba.magdy@mau.edu.eg
                gaberbatiha@gmail.com , dr_gaber_batiha@vetmed.dmu.edu.eg
                Journal
                Thyroid Res
                Thyroid Res
                Thyroid Research
                BioMed Central (London )
                1756-6614
                17 June 2024
                17 June 2024
                2024
                : 17
                : 13
                Affiliations
                [1 ]Assistant Professor, Internal Medicine and Endocrinology, Department of Medicine, College of Medicine, Jouf University, ( https://ror.org/02zsyt821) Sakakah, 04631 Kingdom of Saudi Arabia
                [2 ]Department of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, ( https://ror.org/05s04wy35) Baghdad, Iraq
                [3 ]Department of Medicine, Prince Mohammed Bin Abdulaziz Medical City, Al Jouf-Sakkaka, 42421 Saudi Arabia
                [4 ]University Centre for Research & Development, Chandigarh University, ( https://ror.org/05t4pvx35) Chandigarh-Ludhiana Highway, Mohali, Punjab India
                [5 ]Department of Research & Development, Funogen, Athens, Greece
                [6 ]Department of Research & Development, AFNP Med, Vienna, 1030 Austria
                [7 ]Department of Science and Engineering, Novel Global Community Educational Foundation, Hebersham, 2770 NSW Australia
                [8 ]Department of Surgery II, University Hospital Witten-Herdecke, University of Witten-Herdecke, ( https://ror.org/00yq55g44) Heusnerstrasse 40, Wuppertal, 42283 Germany
                [9 ]Department of Pathology, Faculty of Veterinary Medicine, Matrouh University, Marsa Matruh, 51744 Egypt
                [10 ]Department of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhour University, ( https://ror.org/03svthf85) Damanhour, 22511 AlBeheira Egypt
                Author information
                http://orcid.org/0000-0002-2206-7236
                Article
                199
                10.1186/s13044-024-00199-3
                11181570
                38880884
                e4bf2ec5-0b5f-4750-94ea-e39e3acd6231
                © The Author(s) 2024

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                : 25 September 2023
                : 8 May 2024
                Funding
                Funded by: Private Universität Witten/Herdecke gGmbH (3128)
                Categories
                Review
                Custom metadata
                © BioMed Central Ltd., part of Springer Nature 2024

                Endocrinology & Diabetes
                primary hypothyroidism,atherosclerosis,thyroid stimulating hormone

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