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      Cellular Senescence Affects Cardiac Regeneration and Repair in Ischemic Heart Disease

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          Abstract

          Ischemic heart disease (IHD) is defined as a syndrome of ischemic cardiomyopathy. Myogenesis and angiogenesis in the ischemic myocardium are important for cardiomyocyte (CM) survival, improving cardiac function and decreasing the progression of heart failure after IHD. Cellular senescence is a state of permanent irreversible cell cycle arrest caused by stress that results in a decline in cellular functions, such as proliferation, migration, homing, and differentiation. In addition, senescent cells produce the senescence-associated secretory phenotype (SASP), which affects the tissue microenvironment and surrounding cells by secreting proinflammatory cytokines, chemokines, growth factors, and extracellular matrix degradation proteins. The accumulation of cardiovascular-related senescent cells, including vascular endothelial cells (VECs), vascular smooth muscle cells (VSMCs), CMs and progenitor cells, is an important risk factor of cardiovascular diseases, such as vascular aging, atherosclerotic plaque formation, myocardial infarction (MI) and ventricular remodeling. This review summarizes the processes of angiogenesis, myogenesis and cellular senescence after IHD. In addition, this review focuses on the relationship between cellular senescence and cardiovascular disease and the mechanism of cellular senescence. Finally, we discuss a potential therapeutic strategy for MI targeting senescent cells.

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          The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs

          Yi-Yi Zhu, Tamara Tchkonia, Tamar Pirtskhalava … (2015)
          The healthspan of mice is enhanced by killing senescent cells using a transgenic suicide gene. Achieving the same using small molecules would have a tremendous impact on quality of life and the burden of age-related chronic diseases. Here, we describe the rationale for identification and validation of a new class of drugs termed senolytics, which selectively kill senescent cells. By transcript analysis, we discovered increased expression of pro-survival networks in senescent cells, consistent with their established resistance to apoptosis. Using siRNA to silence expression of key nodes of this network, including ephrins (EFNB1 or 3), PI3Kδ, p21, BCL-xL, or plasminogen-activated inhibitor-2, killed senescent cells, but not proliferating or quiescent, differentiated cells. Drugs targeting these same factors selectively killed senescent cells. Dasatinib eliminated senescent human fat cell progenitors, while quercetin was more effective against senescent human endothelial cells and mouse BM-MSCs. The combination of dasatinib and quercetin was effective in eliminating senescent MEFs. In vivo, this combination reduced senescent cell burden in chronologically aged, radiation-exposed, and progeroid Ercc1 −/Δ mice. In old mice, cardiac function and carotid vascular reactivity were improved 5 days after a single dose. Following irradiation of one limb in mice, a single dose led to improved exercise capacity for at least 7 months following drug treatment. Periodic drug administration extended healthspan in Ercc1 −/Δ mice, delaying age-related symptoms and pathology, osteoporosis, and loss of intervertebral disk proteoglycans. These results demonstrate the feasibility of selectively ablating senescent cells and the efficacy of senolytics for alleviating symptoms of frailty and extending healthspan.
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            The serial cultivation of human diploid cell strains.

            L Hayflick, P.S. Moorhead (1961)
            Article 0 comments Cited 840 times – based on 0 reviews     Review now
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              Endothelial Cell Dysfunction and the Pathobiology of Atherosclerosis.

              Michael Gimbrone, Guillermo García-Cardeña (2016)
              Dysfunction of the endothelial lining of lesion-prone areas of the arterial vasculature is an important contributor to the pathobiology of atherosclerotic cardiovascular disease. Endothelial cell dysfunction, in its broadest sense, encompasses a constellation of various nonadaptive alterations in functional phenotype, which have important implications for the regulation of hemostasis and thrombosis, local vascular tone and redox balance, and the orchestration of acute and chronic inflammatory reactions within the arterial wall. In this review, we trace the evolution of the concept of endothelial cell dysfunction, focusing on recent insights into the cellular and molecular mechanisms that underlie its pivotal roles in atherosclerotic lesion initiation and progression; explore its relationship to classic, as well as more recently defined, clinical risk factors for atherosclerotic cardiovascular disease; consider current approaches to the clinical assessment of endothelial cell dysfunction; and outline some promising new directions for its early detection and treatment.
              Article 0 comments Cited 822 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Aging Dis
                Journal ID (iso-abbrev): Aging Dis
                Title: Aging and Disease
                Publisher: JKL International LLC
                ISSN (Electronic): 2152-5250
                Publication date Collection: April 2021
                Publication date (Electronic): 1 April 2021
                Volume: 12
                Issue: 2
                Pages: 552-569
                Affiliations
                [1-ad-12-2-552] 1Department of Geriatric Cardiology, The First Affiliated Hospital of Guangxi Medical University, Guangxi, China.
                [2-ad-12-2-552] 2Guangxi Key Laboratory of Precision Medicine in Cardio-cerebrovascular Diseases Control and Prevention, Guangxi, China.
                [3-ad-12-2-552] 3Department of Cardiology, Guangxi Clinical Research Center for Cardio-cerebrovascular Diseases, Guangxi, China.
                [4-ad-12-2-552] 4Department of Cardiology, The People's Hospital of Guangxi Zhuang Autonomous Region, Guangxi, China.
                Author notes
                [* ]Correspondence should be addressed to: Dr. Weiqiang Huang, Department of Geriatric Cardiology, The First Affiliated Hospital of Guangxi Medical University, Guangxi, China. Email: hwq2388@ 123456sina.com.
                Article
                Publisher ID: ad-12-2-552
                DOI: 10.14336/AD.2020.0811
                PMC ID: 7990367
                PubMed ID: 33815882
                SO-VID: 678e48f4-e2a8-4237-b950-635bb6a86bd0
                Copyright © copyright: © 2021 Yan et al.
                License:

                this is an open access article distributed under the terms of the creative commons attribution license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

                History
                Date received : 26 May 2020
                Date revision requested : 9 August 2020
                Date accepted : 11 August 2020
                Categories
                Subject: Review

                Keywords: senescence,ischemic heart disease (ihd),angiogenesis,myogenesis
                Data availability:
                Keywords: senescence, ischemic heart disease (ihd), angiogenesis, myogenesis

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