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Biological basis and treatment of frailty and sarcopenia
Cardiovascular Research ( IF 10.2 ) Pub Date : 2024-06-03 , DOI: 10.1093/cvr/cvae073 Ryosuke Sato 1, 2 , Mirela Vatic 1, 2 , Guilherme Wesley Peixoto da Fonseca 3, 4 , Stefan D Anker 5, 6 , Stephan von Haehling 1, 2
Cardiovascular Research ( IF 10.2 ) Pub Date : 2024-06-03 , DOI: 10.1093/cvr/cvae073 Ryosuke Sato 1, 2 , Mirela Vatic 1, 2 , Guilherme Wesley Peixoto da Fonseca 3, 4 , Stefan D Anker 5, 6 , Stephan von Haehling 1, 2
Affiliation
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.
中文翻译:
虚弱和肌肉减少症的生物学基础和治疗
在老龄化社会中,保持健康预期寿命的重要性已被强调。由于与年龄相关的功能储备下降,虚弱是一种脆弱性和易感性增加的状态,对不良健康结果产生严重影响。骨骼肌质量和功能的下降,也称为肌肉减少症,是身体虚弱发展的关键。虚弱和肌肉减少症不仅在高龄患者中非常普遍,而且在患有心力衰竭 (HF)、癌症或痴呆等加剧病情进展的疾病患者中也非常普遍,HF 患者虚弱和肌肉减少症的患病率分别高达 50-75% 和 19.5-47.3%,导致 1 年死亡率高出 1.5-3 倍。虚弱和肌肉减少症的生物学机制是多因素的、复杂的,并且尚未完全阐明,从 DNA 损伤、蛋白质稳态损伤和表观遗传变化到线粒体功能障碍、细胞衰老和环境因素,其中许多因素与心脏病进一步相关。目前,没有治疗虚弱和肌肉减少症的金标准,但是,越来越多的证据表明,运动训练和营养补充剂的结合可以改善骨骼肌功能和虚弱,并且正在根据潜在的病理生理学设计各种其他疗法。在这篇综述中,我们讨论了虚弱和肌肉减少症与心脏病的关系,并描述了对其生物学机制的最新见解,以及通过运动、饮食和特定疗法进行干预的潜力。
更新日期:2024-06-03
中文翻译:
虚弱和肌肉减少症的生物学基础和治疗
在老龄化社会中,保持健康预期寿命的重要性已被强调。由于与年龄相关的功能储备下降,虚弱是一种脆弱性和易感性增加的状态,对不良健康结果产生严重影响。骨骼肌质量和功能的下降,也称为肌肉减少症,是身体虚弱发展的关键。虚弱和肌肉减少症不仅在高龄患者中非常普遍,而且在患有心力衰竭 (HF)、癌症或痴呆等加剧病情进展的疾病患者中也非常普遍,HF 患者虚弱和肌肉减少症的患病率分别高达 50-75% 和 19.5-47.3%,导致 1 年死亡率高出 1.5-3 倍。虚弱和肌肉减少症的生物学机制是多因素的、复杂的,并且尚未完全阐明,从 DNA 损伤、蛋白质稳态损伤和表观遗传变化到线粒体功能障碍、细胞衰老和环境因素,其中许多因素与心脏病进一步相关。目前,没有治疗虚弱和肌肉减少症的金标准,但是,越来越多的证据表明,运动训练和营养补充剂的结合可以改善骨骼肌功能和虚弱,并且正在根据潜在的病理生理学设计各种其他疗法。在这篇综述中,我们讨论了虚弱和肌肉减少症与心脏病的关系,并描述了对其生物学机制的最新见解,以及通过运动、饮食和特定疗法进行干预的潜力。