scholarly journals Exercise-Induced Adult Cardiomyocyte Proliferation in Mammals

2021 ◽  
Vol 12 ◽  
Author(s):  
Guo-liang Zhang ◽  
Ming-li Sun ◽  
Xin-an Zhang
Keyword(s):  
Cardiovascular Diseases ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Research Progress ◽  
Proliferative Potential ◽  
Cardiomyocyte Proliferation ◽  
Predisposing Factor ◽  
Adult Cardiomyocytes ◽  
Exercise Induced

Loss of cardiomyocytes is a vital manifestation and predisposing factor of many cardiovascular diseases and will eventually lead to heart failure (HF). On the other hand, adult mammalian cardiomyocytes have a very limited regenerative capacity and cannot achieve self-repair of the myocardium after injury. Therefore, it is necessary to promote regeneration and repair of the myocardium through effective intervention means. Exercise plays an important role in the prevention and rehabilitation of cardiovascular diseases. Exercise can improve ischemia-reperfusion injury, reduce the size of the infarcted area, and improve the quality of life of patients. In addition, exercise has also been shown to be able to elevate the proliferative potential of adult cardiomyocytes and promote myocardial regeneration. Studies have shown that newly formed cardiomyocytes in adult mammalian hearts are mainly derived from pre-existing cardiomyocytes. By regulating various cytokines, transcription factors, and microRNAs (miRNAs), exercise can promote the dedifferentiation and proliferation of pre-existing cardiomyocytes to form new cardiomyocytes. Therefore, this paper focuses on the recent research progress of exercise-induced adult cardiomyocyte proliferation and explores its potential molecular mechanism.

A Review of Research Progress on Agathis dammara and Its Application Prospects for Cardiovascular Diseases and Fatty Liver Disease

2020 ◽  
Vol 20 ◽  
Author(s):  
Anyi Wang ◽  
Shanshan Yue ◽  
Ankang Peng ◽  
Rong Qi
Keyword(s):  
Liver Disease ◽  
Cardiovascular Diseases ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Modern Society ◽  
Research Progress ◽  
Myocardial Ischemia Reperfusion ◽  
Application Prospects

: Cardiovascular diseases and fatty liver disease have become the leading causes of death in modern society. However, currently existing drugs do not solve all issues related to these diseases; thus, it is expected that more potential drugs for clinical use will be developed. Undeniably, natural products have attracted increasing attention. It is of great significance to identify effective active monomer components for drug discovery and disease prevention. As a pure natural product, Agathis dammara (AD) has antioxidant, hypolipidemic, hypoglycemic, antitumor and anti-inflammatory activities. However, at present, there are few reports regarding the effects of AD on chronic inflammatory cardiovascular diseases such as aneurysm, atherosclerosis, myocardial ischemia-reperfusion injury, and cardiac hypertrophy and liver diseases such as fatty liver disease. AD and products derived from it have very broad application prospects for cardiovascular diseases and fatty liver disease.

scholarly journals New Developments in Exosomal lncRNAs in Cardiovascular Diseases

2021 ◽  
Vol 8 ◽  
Author(s):  
Zhu Yuan ◽  
Weiqiang Huang
Keyword(s):  
Cardiovascular Diseases ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cell Types ◽  
Research Progress ◽  
Therapeutic Effects ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Non Coding Rnas ◽  
Myocardial Ischemia Reperfusion ◽  
Rheumatic Heart

Long non-coding RNAs (lncRNAs) are non-coding RNAs with lengths >200 nt and are involved in the occurrence and development of cardiovascular diseases (CVDs). Exosomes are secreted and produced by various cell types. Exosome contents include various ncRNAs, proteins and lipids. Exosomes are also important mediators of intercellular communication. The proportion of lncRNAs in exosomes is low, but increasing evidence suggests that exosomal lncRNAs play important roles in CVDs. We focused on research progress in exosomal lncRNAs in atherosclerosis, myocardial infarction, myocardial ischemia-reperfusion injury, cardiac angiogenesis, cardiac aging, rheumatic heart disease, and chronic kidney disease combined with CVD. The potential diagnostic and therapeutic effects of exosomal lncRNAs in CVDs are summarized based on preclinical studies involving animal and cell models and circulating exosomes in clinical patients. Finally, the challenges and possible prospects of exosomes and exosomal lncRNAs in clinical applications related to CVD are discussed.

scholarly journals Fundamental Mechanisms of the Cell Death Caused by Nitrosative Stress

2021 ◽  
Vol 9 ◽  
Author(s):  
Fulin Wang ◽  
Qiuhuan Yuan ◽  
Fengying Chen ◽  
Jiaojiao Pang ◽  
Chang Pan ◽  
...  
Keyword(s):  
Cell Death ◽  
Cardiovascular Diseases ◽  
Nitrosative Stress ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Oxygen Metabolism ◽  
The Body ◽  
Practical Significance ◽  
Research Progress ◽  
Metabolism Disorder

Nitrosative stress, as an important oxygen metabolism disorder, has been shown to be closely associated with cardiovascular diseases, such as myocardial ischemia/reperfusion injury, aortic aneurysm, heart failure, hypertension, and atherosclerosis. Nitrosative stress refers to the joint biochemical reactions of nitric oxide (NO) and superoxide (O2–) when an oxygen metabolism disorder occurs in the body. The peroxynitrite anion (ONOO–) produced during this process can nitrate several biomolecules, such as proteins, lipids, and DNA, to generate 3-nitrotyrosine (3-NT), which further induces cell death. Among these, protein tyrosine nitration and polyunsaturated fatty acid nitration are the most studied types to date. Accordingly, an in-depth study of the relationship between nitrosative stress and cell death has important practical significance for revealing the pathogenesis and strategies for prevention and treatment of various diseases, particularly cardiovascular diseases. Here, we review the latest research progress on the mechanisms of nitrosative stress-mediated cell death, primarily involving several regulated cell death processes, including apoptosis, autophagy, ferroptosis, pyroptosis, NETosis, and parthanatos, highlighting nitrosative stress as a unique mechanism in cardiovascular diseases.

Abstract 14391: Transient Cell Cycle Induction in Cardiomyocytes is a Promising Approach to Treat Ischemia Induced Heart Failure

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Riham Abouleisa ◽  
Qinghui Ou ◽  
Xian-liang Tang ◽  
Mitesh Solanki ◽  
Yiru Guo ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cardiac Function ◽  
Single Cell ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiomyocyte Proliferation ◽  
Specific Expression ◽  
Control Virus

Rationale: The regenerative capacity of the heart to repair itself after myocardial infarction (MI)is limited. Our previous study showed that ectopic introduction of Cdk1/CyclinB1 andCdk4/CyclinD1 complexes (4F) promotes cardiomyocyte proliferation in vitro and in vivo andimproves cardiac function after MI. However, its clinical application is limited due to the concernsfor tumorigenic potential in other organs. Objectives: To first, identify on a single cell transcriptomic basis the necessary reprogrammingsteps that cardiomyocytes need to undertake to progress through the proliferation processfollowing 4F overexpression, and then, to determine the pre-clinical efficacy of transient andcardiomyocyte specific expression of 4F in improving cardiac function after MI in small and largeanimals. Methods and Results: Temporal bulk and single cell RNAseq of mature hiPS-CMs treated with4F or LacZ control for 24, 48, or 72 h revealed full cell cycle reprogramming in 15% of thecardiomyocyte population which was associated with sarcomere disassembly and metabolicreprogramming. Transient overexpression of 4F specifically in cardiomyocytes was achievedusing non-integrating lentivirus (NIL) driven by TNNT2 (TNNT2-4F-NIL). One week after inductionof ischemia-reperfusion injury in rats or pigs, TNNT2-4F-NIL or control virus was injectedintramyocardially. Compared with controls, rats or pigs treated with TNNT2-4F-NIL showed a 20-30% significant improvement in ejection fraction and scar size four weeks after treatment, asassessed by echocardiography and histological analysis. Quantification of cardiomyocyteproliferation in pigs using a novel cytokinesis reporter showed that ~10% of the cardiomyocyteswithin the injection site were labelled as daughter cells following injection with TNNT2-4F-NILcompared with ~0.5% background labelling in control groups. Conclusions: We provide the first understanding of the process of forced cardiomyocyteproliferation and advanced the clinical applicability of this approach through minimization ofoncogenic potential of the cell cycle factors using a novel transient and cardiomyocyte-specificviral construct.

scholarly journals Exercise Provides Direct Biphasic Cardioprotection via Manganese Superoxide Dismutase Activation

1999 ◽  
Vol 189 (11) ◽  
pp. 1699-1706 ◽  
Author(s):  
Nobushige Yamashita ◽  
Shiro Hoshida ◽  
Kinya Otsu ◽  
Michio Asahi ◽  
Tsunehiko Kuzuya ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Neutralizing Antibodies ◽  
Time Course ◽  
Manganese Superoxide Dismutase ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Sod Activity ◽  
Manganese Superoxide ◽  
Tnf Α ◽  
Exercise Induced

Epidemiologic investigations have shown that exercise reduces morbidity and mortality from coronary artery disease. In this study, using a rat model, we attempted to determine whether exercise can reduce ischemic injury to the heart and elucidate a mechanism for the cardioprotective effect of exercise. Results showed that exercise significantly reduced the magnitude of a myocardial infarction in biphasic manner. The time course for cardioprotection resembled that of the change in manganese superoxide dismutase (Mn-SOD) activity. The administration of the antisense oligodeoxyribonucleotide to Mn-SOD abolished the expected decrease in infarct size. We showed that the level of tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) increased after exercise. The simultaneous administration of the neutralizing antibodies to the cytokines abolished the exercise-induced cardioprotection and the activation of Mn-SOD. Furthermore, TNF-α can mimic the biphasic pattern of cardioprotection and activation of Mn-SOD. An antioxidant completely abolished cardioprotection and the activation of Mn-SOD by exercise or the injection of TNF-α as well as exercise-induced increase in TNF-α and IL-1β. The production of reactive oxygen species and endogenous TNF-α and IL-1β induced by exercise leads to the activation of Mn-SOD, which plays major roles in the acquisition of biphasic cardioprotection against ischemia/reperfusion injury in rats.

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