cardiac aging
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Author(s):  
Amber Naz ◽  
Shasha Zhang ◽  
Lin An ◽  
Zongpei Song ◽  
Zhenguo Zi ◽  
...  

2021 ◽  
Vol 60 ◽  
pp. 291-297
Author(s):  
Zisong Wei ◽  
Hua Chai ◽  
Yan Chen ◽  
Yue Cheng ◽  
Xiaojing Liu

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1269
Author(s):  
Ramy K. A. Sayed ◽  
Marisol Fernández-Ortiz ◽  
Ibtissem Rahim ◽  
José Fernández-Martínez ◽  
Paula Aranda-Martínez ◽  
...  

To investigate the role of NLRP3 inflammasome in cardiac aging, we evaluate here morphological and ultrastructural age-related changes of cardiac muscles fibers in wild-type and NLRP3-knockout mice, as well as studying the beneficial effect of melatonin therapy. The results clarified the beginning of the cardiac sarcopenia at the age of 12 months, with hypertrophy of cardiac myocytes, increased expression of β-MHC, appearance of small necrotic fibers, decline of cadiomyocyte number, destruction of mitochondrial cristae, appearance of small-sized residual bodies, and increased apoptotic nuclei ratio. These changes were progressed in the cardiac myocytes of 24 old mice, accompanied by excessive collagen deposition, higher expressions of IL-1α, IL-6, and TNFα, complete mitochondrial vacuolation and damage, myofibrils disorganization, multivesicular bodies formation, and nuclear fragmentation. Interestingly, cardiac myocytes of NLRP3−/− mice showed less detectable age-related changes compared with WT mice. Oral melatonin therapy preserved the normal cardiomyocytes structure, restored cardiomyocytes number, and reduced β-MHC expression of cardiac hypertrophy. In addition, melatonin recovered mitochondrial architecture, reduced apoptosis and multivesicular bodies’ formation, and decreased expressions of β-MHC, IL-1α, and IL-6. Fewer cardiac sarcopenic changes and highly remarkable protective effects of melatonin treatment detected in aged cardiomyocytes of NLRP3−/− mice compared with aged WT animals, confirming implication of the NLRP3 inflammasome in cardiac aging. Thus, NLRP3 suppression and melatonin therapy may be therapeutic approaches for age-related cardiac sarcopenia.


2021 ◽  
pp. 111508
Author(s):  
Anna Picca ◽  
Riccardo Calvani ◽  
Hélio José Coelho-Júnior ◽  
Emanuele Marzetti

Author(s):  
Gabor Czibik ◽  
Zaineb Mezdari ◽  
Dogus Murat Altintas ◽  
Juliette Bréhat ◽  
Maria Pini ◽  
...  

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 (Phe) and how it may promote age-related cardiac dysfunction. Methods: We studied cardiac structure and function, together with Phe catabolism in wild-type (WT) and p21 -/- mice (male; 2 to 24 months), the latter known to be protected from cellular senescence. To explore Phe's effects on cellular senescence and ectopic Phe catabolism we treated cardiomyocytes (primary adult rat or human AC-16) with Phe. To establish a role for Phe in driving cardiac aging, WT male mice were treated twice a day with Phe (200 mg/kg) for a month. We also treated aged WT mice with tetrahydrobiopterin (BH4; 10 mg/kg), the essential cofactor for the Phe-degrading enzyme phenylalanine hydroxylase (PAH), or restricted dietary Phe intake. The impact of senescence on hepatic Phe catabolism was explored in vitro in AML12 hepatocytes treated with Nutlin3a (a p53 activator), with or without p21-targeting siRNA or BH4, with quantification of PAH and tyrosine levels. Results: Natural aging is associated with a progressive increase in plasma Phe levels concomitant with cardiac dysfunction, whilst p21 deletion delayed these changes. Phe treatment induced premature cardiac deterioration in young WT mice, strikingly akin to that occurring with aging, whilst triggering cellular senescence, redox and epigenetic changes. Pharmacological restoration of Phe catabolism with BH4 administration or dietary Phe restriction abrogated the rise in plasma Phe and reversed cardiac senescent alterations in aged WT mice. Observations from aged mice and human samples implicated age-related decline in hepatic Phe catabolism as a key driver of elevated plasma Phe levels and showed increased myocardial PAH-mediated Phe catabolism, a novel signature of cardiac aging. Conclusions: Our findings establish a pathogenic role for increased Phe levels in cardiac aging, linking plasma Phe levels to cardiac senescence via dysregulated Phe catabolism along a hepatic-cardiac axis. They highlight Phe/PAH modulation as a potential therapeutic strategy for age-associated cardiac impairment.


Diabetes ◽  
2021 ◽  
Vol 70 (Supplement 1) ◽  
pp. 499-P
Author(s):  
CHANISA THONUSIN ◽  
PATCHARAPONG PANTIYA ◽  
NATTICHA SUMNEANG ◽  
SIRAWIT SRIWICHAIIN ◽  
NIPON CHATTIPAKORN ◽  
...  

Steroids ◽  
2021 ◽  
Vol 170 ◽  
pp. 108829
Author(s):  
Lili Ye ◽  
Jianming Huang ◽  
Xiuting Xiang ◽  
Shicong Song ◽  
Guanshen Huang ◽  
...  
Keyword(s):  

2021 ◽  
Vol 12 ◽  
Author(s):  
Thomas Sithara ◽  
Konstantinos Drosatos

Aging is a process that can be accompanied by molecular and cellular alterations that compromise cardiac function. Although other metabolic disorders with increased prevalence in aged populations, such as diabetes mellitus, dyslipidemia, and hypertension, are associated with cardiovascular complications; aging-related cardiomyopathy has some unique features. Healthy hearts oxidize fatty acids, glucose, lactate, ketone bodies, and amino acids for producing energy. Under physiological conditions, cardiac mitochondria use fatty acids and carbohydrate mainly to generate ATP, 70% of which is derived from fatty acid oxidation (FAO). However, relative contribution of nutrients in ATP synthesis is altered in the aging heart with glucose oxidation increasing at the expense of FAO. Cardiac aging is also associated with impairment of mitochondrial abundance and function, resulting in accumulation of reactive oxygen species (ROS) and activation of oxidant signaling that eventually leads to further mitochondrial damage and aggravation of cardiac function. This review summarizes the main components of pathophysiology of cardiac aging, which pertain to cardiac metabolism, mitochondrial function, and systemic metabolic changes that affect cardiac function.


Author(s):  
Ashley Francois ◽  
Alessandro Canella ◽  
Lynn Marcho ◽  
Matthew S. Stratton

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Mingjing Yan ◽  
Shenghui Sun ◽  
Kun Xu ◽  
Xiuqing Huang ◽  
Lin Dou ◽  
...  

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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