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      The role of cardiac resident macrophage in cardiac aging

      review-article

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          Abstract

          Advancements in longevity research have provided insights into the impact of cardiac aging on the structural and functional aspects of the heart. Notable changes include the gradual remodeling of the myocardium, the occurrence of left ventricular hypertrophy, and the decline in both systolic and diastolic functions. Macrophages, a type of immune cell, play a pivotal role in innate immunity by serving as vigilant agents against pathogens, facilitating wound healing, and orchestrating the development of targeted acquired immune responses. Distinct subsets of macrophages are present within the cardiac tissue and demonstrate varied functions in response to myocardial injury. The differentiation of cardiac macrophages according to their developmental origin has proven to be a valuable strategy in identifying reparative macrophage populations, which originate from embryonic cells and reside within the tissue, as well as inflammatory macrophages, which are derived from monocytes and recruited to the heart. These subsets of macrophages possess unique characteristics and perform distinct functions. This review aims to summarize the current understanding of the roles and phenotypes of cardiac macrophages in various conditions, including the steady state, aging, and other pathological conditions. Additionally, it will highlight areas that require further investigation to expand our knowledge in this field.

          Abstract

          Advancements in modern medicine have significantly increased lifespan, as we age, the functionality of many of our organ systems begins to decline, such as the heart. The differentiation of cardiac macrophages (CCR2− and CCR2+ populations) recruited to the heart, maintaining the physiological processes of heart including neonatal regeneration and adoptive remodeling. During the aging process, specific macrophage subpopulation possess unique characteristics and perform distinct functions.

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          Most cited references161

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          Heart Disease and Stroke Statistics—2017 Update: A Report From the American Heart Association

          Circulation, 135(10)
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            Exploring the full spectrum of macrophage activation.

            Macrophages display remarkable plasticity and can change their physiology in response to environmental cues. These changes can give rise to different populations of cells with distinct functions. In this Review we suggest a new grouping of macrophage populations based on three different homeostatic activities - host defence, wound healing and immune regulation. We propose that similarly to primary colours, these three basic macrophage populations can blend into various other 'shades' of activation. We characterize each population and provide examples of macrophages from specific disease states that have the characteristics of one or more of these populations.
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              Fate mapping analysis reveals that adult microglia derive from primitive macrophages.

              Microglia are the resident macrophages of the central nervous system and are associated with the pathogenesis of many neurodegenerative and brain inflammatory diseases; however, the origin of adult microglia remains controversial. We show that postnatal hematopoietic progenitors do not significantly contribute to microglia homeostasis in the adult brain. In contrast to many macrophage populations, we show that microglia develop in mice that lack colony stimulating factor-1 (CSF-1) but are absent in CSF-1 receptor-deficient mice. In vivo lineage tracing studies established that adult microglia derive from primitive myeloid progenitors that arise before embryonic day 8. These results identify microglia as an ontogenically distinct population in the mononuclear phagocyte system and have implications for the use of embryonically derived microglial progenitors for the treatment of various brain disorders.
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                Author and article information

                Contributors
                xueer09@163.com
                lhw19656@sina.com
                Journal
                Aging Cell
                Aging Cell
                10.1111/(ISSN)1474-9726
                ACEL
                Aging Cell
                John Wiley and Sons Inc. (Hoboken )
                1474-9718
                1474-9726
                10 October 2023
                December 2023
                : 22
                : 12 ( doiID: 10.1111/acel.v22.12 )
                : e14008
                Affiliations
                [ 1 ] Department of Cardiology, Cardiovascular Center, Beijing Friendship Hospital Capital Medical University Beijing China
                [ 2 ] Laboratory for Clinical Medicine Beijing Friendship Hospital, Capital Medical University Beijing China
                [ 3 ] Beijing Key Laboratory of Metabolic Disorder Related Cardiovascular Disease Beijing China
                Author notes
                [*] [* ] Correspondence

                Hongwei Li and Weiping Li, Department of Cardiology, Beijing Friendship Hospital, Capital Medical University, No. 95 Yong'an Road, Xicheng District, Beijing 100050, China.

                Email: lhw19656@ 123456sina.com and xueer09@ 123456163.com

                Author information
                https://orcid.org/0000-0002-1405-0733
                Article
                ACEL14008 ACE-23-0537-MR.R1
                10.1111/acel.14008
                10726886
                37817547
                a3f2f3e0-7b3d-4c7c-87f8-db5e9deade4d
                © 2023 The Authors. Aging Cell published by Anatomical Society and John Wiley & Sons Ltd.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 20 September 2023
                : 18 July 2023
                : 22 September 2023
                Page count
                Figures: 5, Tables: 0, Pages: 18, Words: 15086
                Funding
                Funded by: National Key R&D Program of China
                Award ID: 2021ZD0111000
                Funded by: National Natural Science Foundation of China , doi 10.13039/501100001809;
                Award ID: 82070357
                Categories
                Mini Review
                Mini Reviews
                Custom metadata
                2.0
                December 2023
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.3.6 mode:remove_FC converted:18.12.2023

                Cell biology
                aging,heart,immunity,macrophage
                Cell biology
                aging, heart, immunity, macrophage

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