Artykuły w czasopismach: „Aging cardiac”

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Wessells, Robert J., i Rolf Bodmer. "Cardiac aging". Seminars in Cell & Developmental Biology 18, nr 1 (luty 2007): 111–16. http://dx.doi.org/10.1016/j.semcdb.2006.12.011.

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Li, Zhen, i David J. Lefer. "Demystifying Cardiac Aging". Circulation Research 128, nr 4 (19.02.2021): 508–10. http://dx.doi.org/10.1161/circresaha.121.318741.

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LIMACHER, MARIAN C. "Aging and Cardiac Function". Southern Medical Journal 87, nr 5 (maj 1994): S17. http://dx.doi.org/10.1097/00007611-199405000-00003.

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LIMACHER, MARIAN C. "Aging and Cardiac Function". Southern Medical Journal 87, Supplement (maj 1994): S17. http://dx.doi.org/10.1097/00007611-199405001-00003.

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Miyamoto, Shigeki. "Autophagy and cardiac aging". Cell Death & Differentiation 26, nr 4 (28.01.2019): 653–64. http://dx.doi.org/10.1038/s41418-019-0286-9.

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Renlund, Dale G., i Gary Gerstenblith. "Aging and cardiac function". International Journal of Cardiology 10, nr 3 (marzec 1986): 193–96. http://dx.doi.org/10.1016/0167-5273(86)90001-x.

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Czuriga, D., Z. Papp, I. Czuriga i Á. Balogh. "Cardiac aging – a review". European Surgery 43, nr 2 (kwiecień 2011): 69–77. http://dx.doi.org/10.1007/s10353-011-0600-3.

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Obas, Vanessa, i Ramachandran S. Vasan. "The aging heart". Clinical Science 132, nr 13 (9.07.2018): 1367–82. http://dx.doi.org/10.1042/cs20171156.

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As the elderly segment of the world population increases, it is critical to understand the changes in cardiac structure and function during the normal aging process. In this review, we outline the key molecular pathways and cellular processes that underlie the phenotypic changes in the heart and vasculature that accompany aging. Reduced autophagy, increased mitochondrial oxidative stress, telomere attrition, altered signaling in insulin-like growth factor, growth differentiation factor 11, and 5′- AMP-activated protein kinase pathways are among the key molecular mechanisms underlying cardiac aging. Aging promotes structural and functional changes in the atria, ventricles, valves, myocardium, pericardium, the cardiac conduction system, and the vasculature. We highlight the factors known to accelerate and attenuate the intrinsic aging of the heart and vessels in addition to potential preventive and therapeutic avenues. A greater understanding of the processes involved in cardiac aging may facilitate our ability to mitigate the escalating burden of CVD in older individuals and promote healthy cardiac aging.

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Chen, Bijun, Shuaibo Huang i Nikolaos G. Frangogiannis. "Aging, cardiac repair and Smad3". Aging 10, nr 9 (20.09.2018): 2230–32. http://dx.doi.org/10.18632/aging.101567.

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Westin, Oscar, Finn Gustafsson i Emil Fosbøl. "Occult cardiac amyloidosis?" Aging 11, nr 20 (19.10.2019): 8739–40. http://dx.doi.org/10.18632/aging.102383.

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Ghosh, Asish K. "p300 in Cardiac Development and Accelerated Cardiac Aging". Aging and disease 11, nr 4 (2020): 916. http://dx.doi.org/10.14336/ad.2020.0401.

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尤, 浩鹏. "Research Progress of Cardiac Fibroblasts in Cardiac Aging". Advances in Clinical Medicine 14, nr 07 (2024): 172–78. http://dx.doi.org/10.12677/acm.2024.1471997.

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Hao, Yan, Bohan Li, Sally A. Huber i Wei Liu. "Bibliometric analysis of trends in cardiac aging research over the past 20 years". Medicine 102, nr 34 (25.08.2023): e34870. http://dx.doi.org/10.1097/md.0000000000034870.

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Background: In recent years, many studies have addressed cardiac aging and related diseases. This study aims to understand the research trend of cardiac aging and find new hot issues. Methods: We searched the web of science core collection database for articles published between 2003 and 2022 on the topic of “cardiac aging.” Complete information including keywords, publication year, journal title, country, organization, and author were extracted for analysis. The VOS viewer software was used to generate network maps of keywords, countries, institutions, and author relationships for visual network analysis. Results: A total of 1002 papers were analyzed in the study. Overall, the number of annual publications on cardiac aging has increased since 2009, and new hot topics are emerging. The top 3 countries with the most publications were the United States (471 articles), China (209 articles) and Italy (101 articles). The University of Washington published the most papers (35 articles). The cluster analysis with author as the keyword found that the connections among different scholars are scattered and clustered in a small range. Network analysis based on keyword co-occurrence and year of publication identified relevant features and trends in cardiac aging research. According to the results of cluster analysis, all the articles are divided into 4 topics: “mechanisms of cardiac aging”, “prevention and treatment of cardiac aging”, “characteristics of cardiac aging”, and “others.” In recent years, the mechanism and treatment of cardiac aging have attracted the most attention. In both studies, animal models are used more often than in human populations. Mitochondrial dysfunction, autophagy and mitochondrial autophagy are hotspots in current research. Conclusion: In this study, bibliometric analysis was used to analyze the research trend of cardiac aging in the past 20 years. The mechanism and treatment of cardiac aging are the most concerned contents. Mitochondrial dysfunction, autophagy and mitophagy are the focus of future research on cardiac aging.

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Francois, Ashley, Alessandro Canella, Lynn M. Marcho i Matthew S. Stratton. "Protein acetylation in cardiac aging". Journal of Molecular and Cellular Cardiology 157 (sierpień 2021): 90–97. http://dx.doi.org/10.1016/j.yjmcc.2021.04.007.

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Peters, Colin H., Emily J. Sharpe i Catherine Proenza. "Cardiac Pacemaker Activity and Aging". Annual Review of Physiology 82, nr 1 (10.02.2020): 21–43. http://dx.doi.org/10.1146/annurev-physiol-021119-034453.

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A progressive decline in maximum heart rate (mHR) is a fundamental aspect of aging in humans and other mammals. This decrease in mHR is independent of gender, fitness, and lifestyle, affecting in equal measure women and men, athletes and couch potatoes, spinach eaters and fast food enthusiasts. Importantly, the decline in mHR is the major determinant of the age-dependent decline in aerobic capacity that ultimately limits functional independence for many older individuals. The gradual reduction in mHR with age reflects a slowing of the intrinsic pacemaker activity of the sinoatrial node of the heart, which results from electrical remodeling of individual pacemaker cells along with structural remodeling and a blunted β-adrenergic response. In this review, we summarize current evidence about the tissue, cellular, and molecular mechanisms that underlie the reduction in pacemaker activity with age and highlight key areas for future work.

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Muslin, Anthony J. "New Insights Into Cardiac Aging". Circulation 120, nr 17 (27.10.2009): 1654–56. http://dx.doi.org/10.1161/circulationaha.109.905356.

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Wang, Yuhan, Yujing Li, Chuting He, Bo Gou i Moshi Song. "Mitochondrial regulation of cardiac aging". Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1865, nr 7 (lipiec 2019): 1853–64. http://dx.doi.org/10.1016/j.bbadis.2018.12.008.

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Tocchi, Autumn, Ellen K. Quarles, Nathan Basisty, Lemuel Gitari i Peter S. Rabinovitch. "Mitochondrial dysfunction in cardiac aging". Biochimica et Biophysica Acta (BBA) - Bioenergetics 1847, nr 11 (listopad 2015): 1424–33. http://dx.doi.org/10.1016/j.bbabio.2015.07.009.

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Hao, Yan, i Wei Liu. "Metabolic Changes in Cardiac Aging". Reviews in Cardiovascular Medicine 24, nr 3 (6.03.2023): 82. http://dx.doi.org/10.31083/j.rcm2403082.

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Cianflone, Eleonora, Michele Torella, Cristina Chimenti, Antonella De Angelis, Antonio P. Beltrami, Konrad Urbanek, Marcello Rota i Daniele Torella. "Adult Cardiac Stem Cell Aging: A Reversible Stochastic Phenomenon?" Oxidative Medicine and Cellular Longevity 2019 (7.02.2019): 1–19. http://dx.doi.org/10.1155/2019/5813147.

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Aging is by far the dominant risk factor for the development of cardiovascular diseases, whose prevalence dramatically increases with increasing age reaching epidemic proportions. In the elderly, pathologic cellular and molecular changes in cardiac tissue homeostasis and response to injury result in progressive deteriorations in the structure and function of the heart. Although the phenotypes of cardiac aging have been the subject of intense study, the recent discovery that cardiac homeostasis during mammalian lifespan is maintained and regulated by regenerative events associated with endogenous cardiac stem cell (CSC) activation has produced a crucial reconsideration of the biology of the adult and aged mammalian myocardium. The classical notion of the adult heart as a static organ, in terms of cell turnover and renewal, has now been replaced by a dynamic model in which cardiac cells continuously die and are then replaced by CSC progeny differentiation. However, CSCs are not immortal. They undergo cellular senescence characterized by increased ROS production and oxidative stress and loss of telomere/telomerase integrity in response to a variety of physiological and pathological demands with aging. Nevertheless, the old myocardium preserves an endogenous functionally competent CSC cohort which appears to be resistant to the senescent phenotype occurring with aging. The latter envisions the phenomenon of CSC ageing as a result of a stochastic and therefore reversible cell autonomous process. However, CSC aging could be a programmed cell cycle-dependent process, which affects all or most of the endogenous CSC population. The latter would infer that the loss of CSC regenerative capacity with aging is an inevitable phenomenon that cannot be rescued by stimulating their growth, which would only speed their progressive exhaustion. The resolution of these two biological views will be crucial to design and develop effective CSC-based interventions to counteract cardiac aging not only improving health span of the elderly but also extending lifespan by delaying cardiovascular disease-related deaths.

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Jonnakuti, Sriya T., i Mujib Ullah. "ANTI-AGING PROTEIN CD9 AFFECTS AGE-RELATED HEART FAILURE". Innovation in Aging 3, Supplement_1 (listopad 2019): S255. http://dx.doi.org/10.1093/geroni/igz038.953.

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Abstract The CD9 is transmembrane protein that plays a critical role in many cellular processes including aging associated cardiac pathologies. The heart function declines in the aged population. Ageing is strongly associated with many age-related conditions such as increased risk of heart failure. If aging can be prevented slowed down or even reversed, heart failure and other signs of aging could be controlled or even cured. It is unknown whether CD9 is cardioprotective. The objective of this study is to investigate whether a decline CD9 levels contributes to aging-related heart failure. Our data shows that CD9-deficient aged mice develop cardiac abnormalities and pathological cardiac hypertrophy, Cardioprotection by CD9 in old mice is followed by the downregulation of SIRT6 in the heart, and CD9 overexpressed exosomes ameliorates cardiac pathologies in treated mice and improves their long-term survival. Additionally, the serum level of CD9 decreased significantly in aged mice. CD9 overexpressed exosomes are cardioprotective and improve cardiac function in aged mice. These exosomes mediate their paracrine effects by attenuating, blood pressure, heart beat, reactive oxygen species and fibrosis. Remarkably, CD9 overexpression reversed fibrosis associated brain natriuretic peptide (BNP), Sirt6, and galectin 3 (Gal-3). These results provide a new perspective on the pathogenesis of cardiomyopathies and open new avenues for treatment of the disease.

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Wang, Hui, Yihua Bei, Jing Shi, Junjie Xiao i Xiangqing Kong. "Non-Coding RNAs in Cardiac Aging". Cellular Physiology and Biochemistry 36, nr 5 (2015): 1679–87. http://dx.doi.org/10.1159/000430141.

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Aging has a remarkable impact on the function of the heart, and is independently associated with increased risk for cardiovascular diseases. Cardiac aging is an intrinsic physiological process that results in impaired cardiac function, along with lots of cellular and molecular changes. Non-coding RNAs include small transcripts, such as microRNAs and a wide range of long non-coding RNAs (lncRNAs). Emerging evidence has revealed that non-coding RNAs acted as powerful and dynamic modifiers of cardiac aging. This review aims to provide a general overview of non-coding RNAs implicated in cardiac aging, and the underlying mechanisms involved in maintaining homeo-stasis and retarding aging.

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Gomez-Salinero, Jesus M., Pablo García Pavía i Enrique Lara-Pezzi. "CnAβ1 shifts cardiac metabolism". Aging 11, nr 3 (24.01.2019): 839–40. http://dx.doi.org/10.18632/aging.101789.

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Pagan, Luana U., Mariana J. Gomes, Mariana Gatto, Gustavo A. F. Mota, Katashi Okoshi i Marina P. Okoshi. "The Role of Oxidative Stress in the Aging Heart". Antioxidants 11, nr 2 (9.02.2022): 336. http://dx.doi.org/10.3390/antiox11020336.

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Medical advances and the availability of diagnostic tools have considerably increased life expectancy and, consequently, the elderly segment of the world population. As age is a major risk factor in cardiovascular disease (CVD), it is critical to understand the changes in cardiac structure and function during the aging process. The phenotypes and molecular mechanisms of cardiac aging include several factors. An increase in oxidative stress is a major player in cardiac aging. Reactive oxygen species (ROS) production is an important mechanism for maintaining physiological processes; its generation is regulated by a system of antioxidant enzymes. Oxidative stress occurs from an imbalance between ROS production and antioxidant defenses resulting in the accumulation of free radicals. In the heart, ROS activate signaling pathways involved in myocyte hypertrophy, interstitial fibrosis, contractile dysfunction, and inflammation thereby affecting cell structure and function, and contributing to cardiac damage and remodeling. In this manuscript, we review recent published research on cardiac aging. We summarize the aging heart biology, highlighting key molecular pathways and cellular processes that underlie the redox signaling changes during aging. Main ROS sources, antioxidant defenses, and the role of dysfunctional mitochondria in the aging heart are addressed. As metabolism changes contribute to cardiac aging, we also comment on the most prevalent metabolic alterations. This review will help us to understand the mechanisms involved in the heart aging process and will provide a background for attractive molecular targets to prevent age-driven pathology of the heart. A greater understanding of the processes involved in cardiac aging may facilitate our ability to mitigate the escalating burden of CVD in older individuals and promote healthy cardiac aging.

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Yan, Mingjing, Shenghui Sun, Kun Xu, Xiuqing Huang, Lin Dou, Jing Pang, Weiqing Tang, Tao Shen i Jian Li. "Cardiac Aging: From Basic Research to Therapeutics". Oxidative Medicine and Cellular Longevity 2021 (9.03.2021): 1–13. http://dx.doi.org/10.1155/2021/9570325.

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With research progress on longevity, we have gradually recognized that cardiac aging causes changes in heart structure and function, including progressive myocardial remodeling, left ventricular hypertrophy, and decreases in systolic and diastolic function. Elucidating the regulatory mechanisms of cardiac aging is a great challenge for biologists and physicians worldwide. In this review, we discuss several key molecular mechanisms of cardiac aging and possible prevention and treatment methods developed in recent years. Insights into the process and mechanism of cardiac aging are necessary to protect against age-related diseases, extend lifespan, and reduce the increasing burden of cardiovascular disease in elderly individuals. We believe that research on cardiac aging is entering a new era of unique significance for the progress of clinical medicine and social welfare.

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Lin, Ruizhu, i Risto Kerkelä. "Regulatory Mechanisms of Mitochondrial Function and Cardiac Aging". International Journal of Molecular Sciences 21, nr 4 (18.02.2020): 1359. http://dx.doi.org/10.3390/ijms21041359.

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Aging is a major risk factor for cardiovascular diseases (CVDs), the major cause of death worldwide. Cardiac myocytes, which hold the most abundant mitochondrial population, are terminally differentiated cells with diminished regenerative capacity in the adult. Cardiomyocyte mitochondrial dysfunction is a characteristic feature of the aging heart and one out of the nine features of cellular aging. Aging and cardiac pathologies are also associated with increased senescence in the heart. However, the cause and consequences of cardiac senescence during aging or in cardiac pathologies are mostly unrecognized. Further, despite recent advancement in anti-senescence therapy, the targeted cell type and the effect on cardiac structure and function have been largely overlooked. The unique cellular composition of the heart, and especially the functional properties of cardiomyocytes, need to be considered when designing therapeutics to target cardiac aging. Here we review recent findings regarding key factors regulating cell senescence, mitochondrial health as well as cardiomyocyte rejuvenation.

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Liu, Chang, Xiao Zhang, Meiyu Hu, Yi Lu, Priyanka Gokulnath, Gururaja Vulugundam i Junjie Xiao. "Metabolic targets in cardiac aging and rejuvenation". Journal of Cardiovascular Aging 2, nr 4 (2022): 46. http://dx.doi.org/10.20517/jca.2022.31.

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Cardiac aging is accompanied by progressive loss of cellular function, leading to impaired heart function and heart failure. There is an urgent need for efficient strategies to combat this age-related cardiac dysfunction. A growing number of events suggest that age-related cardiac diseases are tightly related to metabolic imbalance. This review summarizes recent findings concerning metabolic changes during cardiac aging and highlights the therapeutic approaches that target metabolic pathways in cardiac aging.

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Lin, Shenglan, Yana Wang, Xiaojin Zhang, Qiuyue Kong, Chuanfu Li, Yuehua Li, Zhengnian Ding i Li Liu. "HSP27 Alleviates Cardiac Aging in Mice via a Mechanism Involving Antioxidation and Mitophagy Activation". Oxidative Medicine and Cellular Longevity 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/2586706.

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Aging-induced cardiac dysfunction is a prominent feature of cardiac aging. Heat shock protein 27 (HSP27) protects cardiac function against ischemia or chemical challenge. We hypothesized that HSP27 attenuates cardiac aging. Transgenic (Tg) mice with cardiac-specific expression of theHSP27gene and wild-type (WT) littermates were employed in the experiments. Echocardiography revealed a significant decline in the cardiac function of old WT mice compared with young WT mice. In striking contrast, the aging-induced impairment of cardiac function was attenuated in old Tg mice compared with old WT mice. Levels of cardiac aging markers were lower in old Tg mouse hearts than in old WT mouse hearts. Less interstitial fibrosis and lower contents of reactive oxygen species and ubiquitin-conjugated proteins were detected in old Tg hearts than in old WT hearts. Furthermore, old Tg hearts demonstrated lower accumulation of LC3-II and p62 than old WT hearts. Levels of Atg13, Vps34, and Rab7 were also higher in old Tg hearts than in old WT hearts. Additionally, old Tg hearts had higher levels of PINK1 and Parkin than old WT hearts, suggesting that mitophagy was activated in old Tg hearts. Taken together, HSP27 alleviated cardiac aging and this action involved antioxidation and mitophagy activation.

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Cao, Yurou, Shiyi He, Meng Ding, Wenzhi Gu, Tongquan Wang, Shihu Zhang, Jiadong Feng, Qiufang Li i Lan Zheng. "Regular Exercise in Drosophila Prevents Age-Related Cardiac Dysfunction Caused by High Fat and Heart-Specific Knockdown of skd". International Journal of Molecular Sciences 24, nr 2 (7.01.2023): 1216. http://dx.doi.org/10.3390/ijms24021216.

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Skuld (skd) is a subunit of the Mediator complex subunit complex. In the heart, skd controls systemic obesity, is involved in systemic energy metabolism, and is closely linked to cardiac function and aging. However, it is unclear whether the effect of cardiac skd on cardiac energy metabolism affects cardiac function. We found that cardiac-specific knockdown of skd showed impaired cardiac function, metabolic impairment, and premature aging. Drosophila was subjected to an exercise and high-fat diet (HFD) intervention to explore the effects of exercise on cardiac skd expression and cardiac function in HFD Drosophila. We found that Hand-Gal4 > skd RNAi (KC) Drosophila had impaired cardiac function, metabolic impairment, and premature aging. Regular exercise significantly improved cardiac function and metabolism and delayed aging in HFD KC Drosophila. Thus, our study found that the effect of skd on cardiac energy metabolism in the heart affected cardiac function. Exercise may counteract age-related cardiac dysfunction and metabolic disturbances caused by HFD and heart-specific knockdown of skd. Skd may be a potential therapeutic target for heart disease.

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Zhou, Ning, Shaunrick Stoll i Hongyu Qiu. "VCP represses pathological cardiac hypertrophy". Aging 9, nr 12 (26.12.2017): 2469–70. http://dx.doi.org/10.18632/aging.101357.

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Quan, Yue, Yanguo Xin, Geer Tian, Junteng Zhou i Xiaojing Liu. "Mitochondrial ROS-Modulated mtDNA: A Potential Target for Cardiac Aging". Oxidative Medicine and Cellular Longevity 2020 (27.03.2020): 1–11. http://dx.doi.org/10.1155/2020/9423593.

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Mitochondrial DNA (mtDNA) damage is associated with the development of cardiovascular diseases. Cardiac aging plays a central role in cardiovascular diseases. There is accumulating evidence linking cardiac aging to mtDNA damage, including mtDNA mutation and decreased mtDNA copy number. Current wisdom indicates that mtDNA is susceptible to damage by mitochondrial reactive oxygen species (mtROS). This review presents the cellular and molecular mechanisms of cardiac aging, including autophagy, chronic inflammation, mtROS, and mtDNA damage, and the effects of mitochondrial biogenesis and oxidative stress on mtDNA. The importance of nucleoid-associated proteins (Pol γ), nuclear respiratory factors (NRF1 and NRF2), the cGAS-STING pathway, and the mitochondrial biogenesis pathway concerning the development of mtDNA damage during cardiac aging is discussed. Thus, the repair of damaged mtDNA provides a potential clinical target for preventing cardiac aging.

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&NA;. "Renin-Angiotensin System and Cardiac Aging". Drugs & Aging 11, nr 3 (wrzesień 1997): 253. http://dx.doi.org/10.2165/00002512-199711030-00010.

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Cannon, Leah, Alexander C. Zambon, Anthony Cammarato, Zhi Zhang, Georg Vogler, Matthew Munoz, Erika Taylor i in. "Expression patterns of cardiac aging inDrosophila". Aging Cell 16, nr 1 (16.01.2017): 82–92. http://dx.doi.org/10.1111/acel.12559.

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Ice, Randy, Diane Ice i Larry Cahalin. "Case Study The Aging Cardiac Athlete". Cardiopulmonary Physical Therapy Journal 7, nr 1 (1996): 12–15. http://dx.doi.org/10.1097/01823246-199607010-00004.

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Cleveland, Joseph C. "Frailty, Aging, and Cardiac Surgery Outcomes". Journal of the American College of Cardiology 56, nr 20 (listopad 2010): 1677–78. http://dx.doi.org/10.1016/j.jacc.2010.07.021.

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Capogrossi, Maurizio C. "Cardiac Stem Cells Fail With Aging". Circulation Research 94, nr 4 (5.03.2004): 411–13. http://dx.doi.org/10.1161/01.res.0000122070.37999.1b.

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Carbonin, P. U., M. Di Gennaro, M. Pahor, R. Bernabei, A. Sgadari i G. Gambassi. "Cardiac aging, calcium overload, and arrhythmias". Experimental Gerontology 25, nr 3-4 (styczeń 1990): 261–68. http://dx.doi.org/10.1016/0531-5565(90)90061-6.

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Quarles, Ellen K., Dao-Fu Dai, Autumn Tocchi, Nathan Basisty, Lemuel Gitari i Peter S. Rabinovitch. "Quality control systems in cardiac aging". Ageing Research Reviews 23 (wrzesień 2015): 101–15. http://dx.doi.org/10.1016/j.arr.2015.02.003.

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Singam, Narayana Sarma V., Christopher Fine i Jerome L. Fleg. "Cardiac changes associated with vascular aging". Clinical Cardiology 43, nr 2 (16.12.2019): 92–98. http://dx.doi.org/10.1002/clc.23313.

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Czibik, Gabor, Zaineb Mezdari, Dogus Murat Altintas, Juliette Bréhat, Maria Pini, Thomas d’Humières, Thaïs Delmont i in. "Dysregulated Phenylalanine Catabolism Plays a Key Role in the Trajectory of Cardiac Aging". Circulation 144, nr 7 (17.08.2021): 559–74. http://dx.doi.org/10.1161/circulationaha.121.054204.

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Background: Aging myocardium undergoes progressive cardiac hypertrophy and interstitial fibrosis with diastolic and systolic dysfunction. Recent metabolomics studies shed light on amino acids in aging. The present study aimed to dissect how aging leads to elevated plasma levels of the essential amino acid phenylalanine and how it may promote age-related cardiac dysfunction. Methods: We studied cardiac structure and function, together with phenylalanine catabolism in wild-type (WT) and p21 −/− mice (male; 2–24 months), with the latter known to be protected from cellular senescence. To explore phenylalanine’s effects on cellular senescence and ectopic phenylalanine catabolism, we treated cardiomyocytes (primary adult rat or human AC-16) with phenylalanine. To establish a role for phenylalanine in driving cardiac aging, WT male mice were treated twice a day with phenylalanine (200 mg/kg) for a month. We also treated aged WT mice with tetrahydrobiopterin (10 mg/kg), the essential cofactor for the phenylalanine-degrading enzyme PAH (phenylalanine hydroxylase), or restricted dietary phenylalanine intake. The impact of senescence on hepatic phenylalanine catabolism was explored in vitro in AML12 hepatocytes treated with Nutlin3a (a p53 activator), with or without p21-targeting small interfering RNA or tetrahydrobiopterin, with quantification of PAH and tyrosine levels. Results: Natural aging is associated with a progressive increase in plasma phenylalanine levels concomitant with cardiac dysfunction, whereas p21 deletion delayed these changes. Phenylalanine treatment induced premature cardiac deterioration in young WT mice, strikingly akin to that occurring with aging, while triggering cellular senescence, redox, and epigenetic changes. Pharmacological restoration of phenylalanine catabolism with tetrahydrobiopterin administration or dietary phenylalanine restriction abrogated the rise in plasma phenylalanine and reversed cardiac senescent alterations in aged WT mice. Observations from aged mice and human samples implicated age-related decline in hepatic phenylalanine catabolism as a key driver of elevated plasma phenylalanine levels and showed increased myocardial PAH-mediated phenylalanine catabolism, a novel signature of cardiac aging. Conclusions: Our findings establish a pathogenic role for increased phenylalanine levels in cardiac aging, linking plasma phenylalanine levels to cardiac senescence via dysregulated phenylalanine catabolism along a hepatic-cardiac axis. They highlight phenylalanine/PAH modulation as a potential therapeutic strategy for age-associated cardiac impairment.

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Vijayakumar, Anupama, Mingyi Wang i Shivakumar Kailasam. "The Senescent Heart—“Age Doth Wither Its Infinite Variety”". International Journal of Molecular Sciences 25, nr 7 (22.03.2024): 3581. http://dx.doi.org/10.3390/ijms25073581.

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Cardiovascular diseases are a leading cause of morbidity and mortality world-wide. While many factors like smoking, hypertension, diabetes, dyslipidaemia, a sedentary lifestyle, and genetic factors can predispose to cardiovascular diseases, the natural process of aging is by itself a major determinant of the risk. Cardiac aging is marked by a conglomerate of cellular and molecular changes, exacerbated by age-driven decline in cardiac regeneration capacity. Although the phenotypes of cardiac aging are well characterised, the underlying molecular mechanisms are far less explored. Recent advances unequivocally link cardiovascular aging to the dysregulation of critical signalling pathways in cardiac fibroblasts, which compromises the critical role of these cells in maintaining the structural and functional integrity of the myocardium. Clearly, the identification of cardiac fibroblast-specific factors and mechanisms that regulate cardiac fibroblast function in the senescent myocardium is of immense importance. In this regard, recent studies show that Discoidin domain receptor 2 (DDR2), a collagen-activated receptor tyrosine kinase predominantly located in cardiac fibroblasts, has an obligate role in cardiac fibroblast function and cardiovascular fibrosis. Incisive studies on the molecular basis of cardiovascular aging and dysregulated fibroblast function in the senescent heart would pave the way for effective strategies to mitigate cardiovascular diseases in a rapidly growing elderly population.

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Taylor, Jacqueline, i Andreas Fischer. "Endothelial cells dictate cardiac fuel source". Aging 11, nr 4 (13.02.2019): 1083–84. http://dx.doi.org/10.18632/aging.101825.

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Herrero, Diego, i Antonio Bernad. "Cardiac progenitors cells for vascular repair". Aging 11, nr 5 (24.02.2019): 1319–20. http://dx.doi.org/10.18632/aging.101840.

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Wang, Shu, Yanan Jiang, Jingling Chen, Changliang Dai, Dandan Liu, Wei Pan, Lijuan Wang i in. "Activation of M3 Muscarinic Acetylcholine Receptors Delayed Cardiac Aging by Inhibiting the Caspase-1/IL-1β Signaling Pathway". Cellular Physiology and Biochemistry 49, nr 3 (2018): 1249–57. http://dx.doi.org/10.1159/000493332.

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Background/Aims: Because the prevalence of age-related cardiac impairment increases as the human lifespan increases, it is important to combat the effects of aging. Recently, the cardiac M3 muscarinic acetylcholine receptor (M3-mAChR) has been demonstrated to play important roles in cardiac development and in the pathogenesis of cardiac diseases. However, the role of M3-mAChR in aging remains largely unknown. Therefore, the aim of this study was to investigate the involvement of M3-mAChR in the progression of cardiac aging. Methods: We established a cardiac aging model in mice through subcutaneous injection with D-galactose at a dose of 100 mg/kg/day for 6 weeks. D-galactose was also used to induce aging in primary cultured neonatal mouse cardiomyocytes. The myocardium from mice was stained with hematoxylin and eosin for histological analysis. The protein expression levels of p53 and p21 were determined using western blotting. The mRNA and protein expression levels of M3-mAChR, caspase-1, and interleukin (IL)-1β were determined using real-time PCR, immunohistochemical staining, and western blotting. Results: The expression of M3-mAChR was down-regulated in the myocardium from aged mice and D-galactose-treated mice, while the expression levels of caspase-1 and its downstream molecule IL-1β were significantly increased. The M3-mAChR agonist choline reduced the increase in caspase-1 in cardiomyocytes induced by D-galactose, which was reversed by the M3-mAChR antagonist 4-DAMP. Moreover, 4-DAMP promoted D-galactose-induced cardiomyocyte aging, which was attenuated by a caspase-1 inhibitor. Conclusion: Activation of M3-mAChR delayed cardiac aging by inhibiting the caspase-1/IL-1β signaling pathway.

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Putri, Mustika Anggiane, Patwa Amani, Donna Adriani i Rita Khairani. "Importance of Exercise in Mitigating Age-Related Cardiac Apoptosis". Sriwijaya Journal of Medicine 6, nr 3 (20.12.2023): 94–101. http://dx.doi.org/10.32539/sjm.v6i3.208.

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Aging causes a progressive decline in heart function. Loss of cardiomyocytes through programmed cell death or apoptosis is a critical factor contributing to this age-related damage. As we age, the heart undergoes structural changes, such as loss of cardiomyocytes, cardiomyocyte hypertrophy, and increased connective tissue with changes in heart geometry. It is widely known that mitochondria are vital sites of apoptosis. Mitochondrial-mediated apoptotic pathways are important regulators of apoptosis with aging. Mitochondrial dysfunction and oxidative stress also contribute to the cardiac remodeling and apoptosis associated with the aging process. On the other hand, exercise can improve heart function and reduce the risk of heart disease. Recent studies suggest that aging increases apoptotic signaling in the left ventricle. However, chronic exercise reduces this mitochondrial-mediated apoptotic signaling pathway in the aging heart. This review will describe the impacts of aging and exercise on cardiac apoptosis, highlighting the importance of exercise in reducing age-related cardiac apoptosis.

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Li, Qun, Shan Wu, Shi-Yan Li, Faye L. Lopez, Min Du, Jan Kajstura, Piero Anversa i Jun Ren. "Cardiac-specific overexpression of insulin-like growth factor 1 attenuates aging-associated cardiac diastolic contractile dysfunction and protein damage". American Journal of Physiology-Heart and Circulatory Physiology 292, nr 3 (marzec 2007): H1398—H1403. http://dx.doi.org/10.1152/ajpheart.01036.2006.

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Aging is associated with hepatic growth hormone resistance resulting in a fall in serum insulin-like growth factor 1 (IGF-1) level. However, whether loss of IGF-1 contributes to cardiac aging is unclear. This study was designed to examine the effect of cardiac overexpression of IGF-1 on cardiomyocyte contractile function in young (3 mo) and old (26–28 mo) mice. Cardiomyocyte contractile function was evaluated, including peak shortening (PS), time to 90% PS, time to 90% relengthening (TR90), and maximal velocity of shortening/relengthening (±d L/d t). Levels of advanced glycation end product, protein carbonyl, sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA2a), phospholamban, and Na+/Ca2+ exchanger were assessed by Western blot analysis. SERCA activity was measured by 45Ca2+ uptake. Aging induced a decline in plasma IGF-1 levels. Aged cells exhibited depressed ±d L/d t, prolonged TR90, and a steeper PS decline in response to increasing stimulus frequency compared with those in young myocytes. IGF-1 transgene alleviated aging-induced loss in plasma IGF-1 and aging-induced mechanical defects with little effect in young mice. The beneficial effect of IGF-1 transgene on aging-associated cardiomyocyte contractile dysfunction was somewhat mimicked by short-term in vitro treatment of recombinant IGF-1 (500 nM). Advanced glycation end product and protein carbonyl levels were higher in aged mice, which were not affected by IGF-1. Expression of SERCA2a (but not Na+/Ca2+ exchanger and phospholamban) and SERCA activity were reduced with aging, which was ablated by the IGF-1 transgene. Collectively, our data suggest a beneficial role of IGF-1 in aging-induced cardiac contractile dysfunction, possibly related to improved Ca2+ uptake.

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Adekunbi, Daniel, Elizabeth Reilly, Sandra Sanchez-Reilly, Cun Li, Peter Nathanielsz, Laura Cox i Adam Salmon. "CELLULAR RESILIENCE AND THE AGING HEART: UNDERSTANDING MITOCHONDRIAL INJURY MECHANISMS USING THE BABOON". Innovation in Aging 7, Supplement_1 (1.12.2023): 1000. http://dx.doi.org/10.1093/geroni/igad104.3214.

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Abstract Background Aging-related cardiovascular disease is deadly worldwide. Cardiac aging in non-human primates (NHP), including baboons, is similar to humans, and intrauterine growth restriction animal models (IUGR) have shown to accelerate cardiac aging and foment cardiomyopathies. Objective: To measure and compare basal and metabolically stressed mitochondrial function among cardiac fibroblasts (CF) isolated from control vs. prematurely older (IUGR) baboons. Methods CF were isolated from IUGR and control baboon hearts under standard conditions (25mM Glucose). Additional subgroups were exposed to Metabolic Stress (MS-exposed to 2-hours of low glucose, 1mM). Mitochondrial Oxygen Consumption Rate (OCR) and extracellular acidification rate (ECAR) were measured via Seahorse XFe96 instrument. Results Donor Age: 13.27 – 17.52 years (elderly baboons), Male/Female data combined, n=4-5. OCR was higher in control relative to IUGR among all groups. ATP demand and non-mitochondrial respiration had similar values between control and IUGR. MS impacted CF bioenergetics similarly in control and IUGR. ECAR was higher in MS cells in both control/IUGR. OCR:ECAR ratio was higher in control vs IUGR while MS lowered OCR:ECAR ratio in control to levels comparable to IUGR. Conclusion Higher OCR indicated increased metabolic demands of aging cells depending on glycolysis for survival. MS significantly impaired mitochondrial function across all cardiac cells regardless of aging. IUGR not only accelerated cardiac aging but impaired basal and metabolic response of CF. CF retain metabolic characteristics of their donor status and represent a cardiac aging model to explore mitochondrial injury mechanisms, understand cellular resilience and subsequently develop protective translational interventions.

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Yeh, Chi-Hsiao, Yi-Ju Chou, Ting-Kuan Chu i Ting-Fen Tsai. "Rejuvenating the Aging Heart by Enhancing the Expression of the Cisd2 Prolongevity Gene". International Journal of Molecular Sciences 22, nr 21 (25.10.2021): 11487. http://dx.doi.org/10.3390/ijms222111487.

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Aging is the major risk factor for cardiovascular disease, which is the leading cause of mortality worldwide among aging populations. Cisd2 is a prolongevity gene that mediates lifespan in mammals. Previously, our investigations revealed that a persistently high level of Cisd2 expression in mice is able to prevent age-associated cardiac dysfunction. This study was designed to apply a genetic approach that induces cardiac-specific Cisd2 overexpression (Cisd2 icOE) at a late-life stage, namely a time point immediately preceding the onset of old age, and evaluate the translational potential of this approach. Several discoveries are pinpointed. Firstly, Cisd2 is downregulated in the aging heart. This decrease in Cisd2 leads to cardiac dysfunction and impairs electromechanical performance. Intriguingly, Cisd2 icOE prevents an exacerbation of age-associated electromechanical dysfunction. Secondly, Cisd2 icOE ameliorates cardiac fibrosis and improves the integrity of the intercalated discs, thereby reversing various structural abnormalities. Finally, Cisd2 icOE reverses the transcriptomic profile of the aging heart, changing it from an older-age pattern to a younger pattern. Intriguingly, Cisd2 icOE modulates a number of aging-related pathways, namely the sirtuin signaling, autophagy, and senescence pathways, to bring about rejuvenation of the heart as it enters old age. Our findings highlight Cisd2 as a novel molecular target for developing therapies targeting cardiac aging.

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Jahangir, Arshad, Sandeep Sagar i Andre Terzic. "Aging and cardioprotection". Journal of Applied Physiology 103, nr 6 (grudzień 2007): 2120–28. http://dx.doi.org/10.1152/japplphysiol.00647.2007.

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Advanced age is a strong independent predictor for death, disability, and morbidity in patients with structural heart disease. With the projected increase in the elderly population and the prevalence of age-related cardiovascular disabilities worldwide, the need to understand the biology of the aging heart, the mechanisms for age-mediated cardiac vulnerability, and the development of strategies to limit myocardial dysfunction in the elderly have never been more urgent. Experimental evidence in animal models indicate attenuation in cardioprotective pathways with aging, yet limited information is available regarding age-related changes in the human heart. Human cardiac aging generates a complex phenotype, only partially replicated in animal models. Here, we summarize current understanding of the aging heart stemming from clinical and experimental studies, and we highlight targets for protection of the vulnerable senescent myocardium. Further progress mandates assessment of human tissue to dissect specific aging-associated genomic and proteomic dynamics, and their functional consequences leading to increased susceptibility of the heart to injury, a critical step toward designing novel therapeutic interventions to limit age-related myocardial dysfunction and promote healthy aging.

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Huang, Pianpian, Lijuan Bai, Lihua Liu, Jun Fu, Kefei Wu, Hongxia Liu, Yun Liu, Benming Qi i Benling Qi. "Redd1 knockdown prevents doxorubicin-induced cardiac senescence". Aging 13, nr 10 (6.05.2021): 13788–806. http://dx.doi.org/10.18632/aging.202972.

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