Biological basis and treatment of frailty and sarcopenia

肌萎缩 医学 痴呆 老年学 疾病 心力衰竭 预期寿命 蛋白质稳态 内科学 人口 生物 环境卫生 遗传学
作者
Ryosuke Sato,Mirela Vatic,Guilherme Wesley Peixoto da Fonseca,Stefan D. Anker,Stephan von Haehling
出处
期刊:Cardiovascular Research [Oxford University Press]
卷期号:120 (9): 982-998
标识
DOI:10.1093/cvr/cvae073
摘要

Abstract In an ageing society, the importance of maintaining healthy life expectancy has been emphasized. As a result of age-related decline in functional reserve, frailty is a state of increased vulnerability and susceptibility to adverse health outcomes with a serious impact on healthy life expectancy. The decline in skeletal muscle mass and function, also known as sarcopenia, is key in the development of physical frailty. Both frailty and sarcopenia are highly prevalent in patients not only with advanced age but also in patients with illnesses that exacerbate their progression like heart failure (HF), cancer, or dementia, with the prevalence of frailty and sarcopenia in HF patients reaching up to 50–75% and 19.5–47.3%, respectively, resulting in 1.5–3 times higher 1-year mortality. The biological mechanisms of frailty and sarcopenia are multifactorial, complex, and not yet fully elucidated, ranging from DNA damage, proteostasis impairment, and epigenetic changes to mitochondrial dysfunction, cellular senescence, and environmental factors, many of which are further linked to cardiac disease. Currently, there is no gold standard for the treatment of frailty and sarcopenia, however, growing evidence supports that a combination of exercise training and nutritional supplement improves skeletal muscle function and frailty, with a variety of other therapies being devised based on the underlying pathophysiology. In this review, we address the involvement of frailty and sarcopenia in cardiac disease and describe the latest insights into their biological mechanisms as well as the potential for intervention through exercise, diet, and specific therapies.
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