Angeliki Vakka, Junco S Warren, Konstantinos Drosatos
Progressive age-induced deterioration in the structure and function of the cardiovascular system involves cardiac hypertrophy, diastolic dysfunction, myocardial fibrosis, arterial stiffness, and endothelial dysfunction. These changes are driven by complex processes that are interconnected, such as oxidative stress, mitochondrial dysfunction, autophagy, inflammation, fibrosis, and telomere dysfunction. In recent years, the advances in research of cardiovascular aging, including the wide use of animal models of cardiovascular aging, elucidated an abundance of cell signaling pathways involved in these processes and brought into sight possible interventions, which span from pharmacological agents, such as metformin, sodium-glucose cotransporter 2-inhibitors, rapamycin, dasatinib and quercetin, to lifestyle changes.
{"title":"Cardiovascular aging: from cellular and molecular changes to therapeutic interventions.","authors":"Angeliki Vakka, Junco S Warren, Konstantinos Drosatos","doi":"10.20517/jca.2023.09","DOIUrl":"https://doi.org/10.20517/jca.2023.09","url":null,"abstract":"<p><p>Progressive age-induced deterioration in the structure and function of the cardiovascular system involves cardiac hypertrophy, diastolic dysfunction, myocardial fibrosis, arterial stiffness, and endothelial dysfunction. These changes are driven by complex processes that are interconnected, such as oxidative stress, mitochondrial dysfunction, autophagy, inflammation, fibrosis, and telomere dysfunction. In recent years, the advances in research of cardiovascular aging, including the wide use of animal models of cardiovascular aging, elucidated an abundance of cell signaling pathways involved in these processes and brought into sight possible interventions, which span from pharmacological agents, such as metformin, sodium-glucose cotransporter 2-inhibitors, rapamycin, dasatinib and quercetin, to lifestyle changes.</p>","PeriodicalId":75051,"journal":{"name":"The journal of cardiovascular aging","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10238104/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9955597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01Epub Date: 2023-03-31DOI: 10.20517/jca.2023.13
Priyatansh Gurha, Nadeem Ishaq, Ali J Marian
{"title":"ChatGPT and other artificial intelligence chatbots and biomedical writing.","authors":"Priyatansh Gurha, Nadeem Ishaq, Ali J Marian","doi":"10.20517/jca.2023.13","DOIUrl":"10.20517/jca.2023.13","url":null,"abstract":"","PeriodicalId":75051,"journal":{"name":"The journal of cardiovascular aging","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10121201/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9382386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Circadian rhythms are 24-h biological rhythms that are necessary for optimal health and daily variances in physiology and behavior. Circadian rhythms are maintained at the cellular level and are necessary for organ-specific functions. Cardiac tissue is no exception, and the heart maintains strong rhythms in gene expression as well as cellular metabolism throughout its lifespan [1] . Aging is associated with the gradual decline of circadian rhythms, raising the question of whether pharmacological or behavioral mechanisms that increase circadian robustness can slow the aging process. Time-restricted feeding is one mechanism to augment internal rhythms, decreased fat mass compared to ad libitum -fed mice); and (3) changes in circulating glucose in aged mice. Specifically, though insulin levels were similar in young AL and CR mice, circulating glucose was decreased in CR, suggesting increased insulin sensitivity. Upon aging, though all CR mice had lower insulin levels, even aged CR mice showed elevations in glucose, similar to AL groups. Thus, CR protects against insulin resistance across the lifespan.
{"title":"The importance of \"when\" in calorie restriction-induced lifespan extension.","authors":"Kristin Eckel-Mahan","doi":"10.20517/jca.2022.40","DOIUrl":"https://doi.org/10.20517/jca.2022.40","url":null,"abstract":"Circadian rhythms are 24-h biological rhythms that are necessary for optimal health and daily variances in physiology and behavior. Circadian rhythms are maintained at the cellular level and are necessary for organ-specific functions. Cardiac tissue is no exception, and the heart maintains strong rhythms in gene expression as well as cellular metabolism throughout its lifespan [1] . Aging is associated with the gradual decline of circadian rhythms, raising the question of whether pharmacological or behavioral mechanisms that increase circadian robustness can slow the aging process. Time-restricted feeding is one mechanism to augment internal rhythms, decreased fat mass compared to ad libitum -fed mice); and (3) changes in circulating glucose in aged mice. Specifically, though insulin levels were similar in young AL and CR mice, circulating glucose was decreased in CR, suggesting increased insulin sensitivity. Upon aging, though all CR mice had lower insulin levels, even aged CR mice showed elevations in glucose, similar to AL groups. Thus, CR protects against insulin resistance across the lifespan.","PeriodicalId":75051,"journal":{"name":"The journal of cardiovascular aging","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9762686/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9151184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Can age be a modifiable risk factor? the impact of dietary patterns on the molecular mechanisms that underlie cardiovascular aging","authors":"","doi":"10.20517/jca.2023.1","DOIUrl":"https://doi.org/10.20517/jca.2023.1","url":null,"abstract":"","PeriodicalId":75051,"journal":{"name":"The journal of cardiovascular aging","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67657368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mitochondrial dynamics is driven by a balance between fusion and fission[1,2]. Fusion connects individual mitochondria to form a network of highly energy-efficient organelle systems. Fission drives fragmentation of the mitochondrial network resulting in less energy-efficient organelles. Nevertheless, fission is critical for the removal of damaged mitochondria and the mitigation of oxidative stress. Well-defined factors that control fusion (mitofusin-1/2, optical atrophy protein-1/2) and fission (dynamin-related protein 1, mitochondrial fusion factor, fission protein 1) regulate mitochondrial connectivity dynamics. Mitochondrial dynamics is critical for energy homeostasis, particularly in the skeletal muscle[1], one of the most plastic organs in adulthood amenable to remodeling by exercise, as well as a sedentary lifestyle and aging[3]. Exercise has long been known to be necessary for healthy aging and energy efficiency, as well as for delaying cardiovascular and metabolic diseases[4]. Exercise benefits are partly mediated by boosting energy metabolism[1]. However, molecular mechanisms of age-related decline in physical fitness, and its counterdelay by exercise, are poorly defined. Skeletal muscle is an excellent organ system for obtaining molecular insights into the interaction between exercise and aging, particularly as it is related to mitochondrial dynamics, muscle quality, and fitness. So far, studies in
{"title":"A worm's life: AMPK links muscle mitochondrial dynamics to physical fitness and healthy aging in <i>Caenorhabditis elegans</i>.","authors":"Vihang A Narkar","doi":"10.20517/jca.2023.14","DOIUrl":"https://doi.org/10.20517/jca.2023.14","url":null,"abstract":"Mitochondrial dynamics is driven by a balance between fusion and fission[1,2]. Fusion connects individual mitochondria to form a network of highly energy-efficient organelle systems. Fission drives fragmentation of the mitochondrial network resulting in less energy-efficient organelles. Nevertheless, fission is critical for the removal of damaged mitochondria and the mitigation of oxidative stress. Well-defined factors that control fusion (mitofusin-1/2, optical atrophy protein-1/2) and fission (dynamin-related protein 1, mitochondrial fusion factor, fission protein 1) regulate mitochondrial connectivity dynamics. Mitochondrial dynamics is critical for energy homeostasis, particularly in the skeletal muscle[1], one of the most plastic organs in adulthood amenable to remodeling by exercise, as well as a sedentary lifestyle and aging[3]. Exercise has long been known to be necessary for healthy aging and energy efficiency, as well as for delaying cardiovascular and metabolic diseases[4]. Exercise benefits are partly mediated by boosting energy metabolism[1]. However, molecular mechanisms of age-related decline in physical fitness, and its counterdelay by exercise, are poorly defined. Skeletal muscle is an excellent organ system for obtaining molecular insights into the interaction between exercise and aging, particularly as it is related to mitochondrial dynamics, muscle quality, and fitness. So far, studies in","PeriodicalId":75051,"journal":{"name":"The journal of cardiovascular aging","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10256235/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9626821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Why the bee in our bonnets about Beethoven's hair?","authors":"P. Libby","doi":"10.20517/jca.2023.17","DOIUrl":"https://doi.org/10.20517/jca.2023.17","url":null,"abstract":"","PeriodicalId":75051,"journal":{"name":"The journal of cardiovascular aging","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67657393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01Epub Date: 2023-01-03DOI: 10.20517/jca.2022.42
Benjamin Werbner, Omid Mohammad Tavakoli-Rouzbehani, Amir Nima Fatahian, Sihem Boudina
This review provides a holistic perspective on the bi-directional relationship between cardiac mitochondrial dysfunction and myocardial structural remodeling in the context of metabolic heart disease, natural cardiac aging, and heart failure. First, a review of the physiologic and molecular drivers of cardiac mitochondrial dysfunction across a range of increasingly prevalent conditions such as metabolic syndrome and cardiac aging is presented, followed by a general review of the mechanisms of mitochondrial quality control (QC) in the heart. Several important mechanisms by which cardiac mitochondrial dysfunction triggers or contributes to structural remodeling of the heart are discussed: accumulated metabolic byproducts, oxidative damage, impaired mitochondrial QC, and mitochondrial-mediated cell death identified as substantial mechanistic contributors to cardiac structural remodeling such as hypertrophy and myocardial fibrosis. Subsequently, the less studied but nevertheless important reverse relationship is explored: the mechanisms by which cardiac structural remodeling feeds back to further alter mitochondrial bioenergetic function. We then provide a condensed pathogenesis of several increasingly important clinical conditions in which these relationships are central: diabetic cardiomyopathy, age-associated declines in cardiac function, and the progression to heart failure, with or without preserved ejection fraction. Finally, we identify promising therapeutic opportunities targeting mitochondrial function in these conditions.
{"title":"The dynamic interplay between cardiac mitochondrial health and myocardial structural remodeling in metabolic heart disease, aging, and heart failure.","authors":"Benjamin Werbner, Omid Mohammad Tavakoli-Rouzbehani, Amir Nima Fatahian, Sihem Boudina","doi":"10.20517/jca.2022.42","DOIUrl":"10.20517/jca.2022.42","url":null,"abstract":"<p><p>This review provides a holistic perspective on the bi-directional relationship between cardiac mitochondrial dysfunction and myocardial structural remodeling in the context of metabolic heart disease, natural cardiac aging, and heart failure. First, a review of the physiologic and molecular drivers of cardiac mitochondrial dysfunction across a range of increasingly prevalent conditions such as metabolic syndrome and cardiac aging is presented, followed by a general review of the mechanisms of mitochondrial quality control (QC) in the heart. Several important mechanisms by which cardiac mitochondrial dysfunction triggers or contributes to structural remodeling of the heart are discussed: accumulated metabolic byproducts, oxidative damage, impaired mitochondrial QC, and mitochondrial-mediated cell death identified as substantial mechanistic contributors to cardiac structural remodeling such as hypertrophy and myocardial fibrosis. Subsequently, the less studied but nevertheless important reverse relationship is explored: the mechanisms by which cardiac structural remodeling feeds back to further alter mitochondrial bioenergetic function. We then provide a condensed pathogenesis of several increasingly important clinical conditions in which these relationships are central: diabetic cardiomyopathy, age-associated declines in cardiac function, and the progression to heart failure, with or without preserved ejection fraction. Finally, we identify promising therapeutic opportunities targeting mitochondrial function in these conditions.</p>","PeriodicalId":75051,"journal":{"name":"The journal of cardiovascular aging","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9894375/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9237341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In the January 13, 2023 issue of Science, Lebek and colleagues demonstrate the potential broad utility of in vivo base editing as a gene therapy for heart disease[1]. Following myocardial infarction, it is a race against time to begin thrombolytic therapy and percutaneous coronary intervention to restore blood flow to the infarcted region. Revascularization of the infarcted artery is performed to prevent cardiomyocyte death, fibrosis, and heart failure. However, these procedures come with their own adverse sequelae of ischemia-reperfusion injuries, which include myocardial stunning, microvascular obstruction, arrhythmias, and lethal injury[2]. Therapies that can either prevent cardiomyocyte injury and death, or promote regeneration of the infarcted tissue are desperately needed. Such approaches should use common molecular pathways that are applicable to all patients.
{"title":"CaMKIIδ gene editing- A base hit for the heart.","authors":"Christopher J Walkey, William R Lagor","doi":"10.20517/jca.2023.11","DOIUrl":"https://doi.org/10.20517/jca.2023.11","url":null,"abstract":"In the January 13, 2023 issue of Science, Lebek and colleagues demonstrate the potential broad utility of in vivo base editing as a gene therapy for heart disease[1]. Following myocardial infarction, it is a race against time to begin thrombolytic therapy and percutaneous coronary intervention to restore blood flow to the infarcted region. Revascularization of the infarcted artery is performed to prevent cardiomyocyte death, fibrosis, and heart failure. However, these procedures come with their own adverse sequelae of ischemia-reperfusion injuries, which include myocardial stunning, microvascular obstruction, arrhythmias, and lethal injury[2]. Therapies that can either prevent cardiomyocyte injury and death, or promote regeneration of the infarcted tissue are desperately needed. Such approaches should use common molecular pathways that are applicable to all patients.","PeriodicalId":75051,"journal":{"name":"The journal of cardiovascular aging","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10104458/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9373143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Exercise induces cardiomyogenesis in the aged heart","authors":"","doi":"10.20517/jca.2023.06","DOIUrl":"https://doi.org/10.20517/jca.2023.06","url":null,"abstract":"","PeriodicalId":75051,"journal":{"name":"The journal of cardiovascular aging","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67657327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"ASGR1 and cholesterol: connecting the dots","authors":"","doi":"10.20517/jca.2023.8","DOIUrl":"https://doi.org/10.20517/jca.2023.8","url":null,"abstract":"","PeriodicalId":75051,"journal":{"name":"The journal of cardiovascular aging","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67657736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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