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Simultaneous Isolation of High Quality Cardiomyocytes, Endothelial Cells, and Fibroblasts from an Adult Rat Heart
Published on: May 19, 2017
Aging and cardioprotection
Arshad Jahangir1, Sandeep Sagar, Andre Terzic
1Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, and Department of Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA. jahangir.arshad@mayo.edu
Insights
As people age, their hearts become more vulnerable to damage, increasing the risk of death and disability from heart disease. Understanding the aging heart is crucial for developing new treatments to protect elderly individuals.
Area of Science:
- Cardiovascular Biology
- Gerontology
- Cardiac Pathophysiology
Background:
- Advanced age is a significant risk factor for mortality and morbidity in structural heart disease.
- The global elderly population is increasing, highlighting the urgent need to understand cardiac aging and vulnerability.
Purpose of the Study:
- To summarize current knowledge on human cardiac aging from clinical and experimental studies.
- To identify targets for protecting the aging myocardium and limiting age-related myocardial dysfunction.
Main Methods:
- Review of clinical and experimental studies on cardiac aging.
- Analysis of age-related genomic and proteomic dynamics in human cardiac tissue.
Main Results:
- Aging attenuates cardioprotective pathways, but human cardiac aging presents a complex phenotype not fully replicated in animal models.
- Specific aging-associated genomic and proteomic changes increase heart susceptibility to injury.
Conclusions:
- Further research on human cardiac tissue is essential to understand aging-related myocardial dysfunction.
- Identifying therapeutic targets is critical for promoting healthy aging and preventing age-related heart disease.
Abstract:
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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