Physical exercise, autophagy and cardiometabolic stress in aging

Tian, Haili; Chen, Peijie; Ren, Jun

doi:10.18632/aging.102129

Cited by 7 publications

(5 citation statements)

References 8 publications

(12 reference statements)

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“…In a recent randomized controlled trial, endurance training and interval training (but not resistance training) were found to promote telomerase activity and telomere length, essential markers for cellular senescence, regenerative capacity, and healthy aging [57]. Moreover, physical exercise appears to exert a favorable effect on aging-related cardiometabolic stress through mediating autophagy [58].…”

Section: Contemporary Theory Behind Exercise-induced Cardiovasculamentioning

confidence: 99%

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Physical Exercise and Selective Autophagy: Benefit and Risk on Cardiovascular Health

Tian

Chen

et al. 2019

Cells

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Physical exercise promotes cardiorespiratory fitness, and is considered the mainstream of non-pharmacological therapies along with lifestyle modification for various chronic diseases, in particular cardiovascular diseases. Physical exercise may positively affect various cardiovascular risk factors including body weight, blood pressure, insulin sensitivity, lipid and glucose metabolism, heart function, endothelial function, and body fat composition. With the ever-rising prevalence of obesity and other types of metabolic diseases, as well as sedentary lifestyle, regular exercise of moderate intensity has been indicated to benefit cardiovascular health and reduce overall disease mortality. Exercise offers a wide cadre of favorable responses in the cardiovascular system such as improved dynamics of the cardiovascular system, reduced prevalence of coronary heart diseases and cardiomyopathies, enhanced cardiac reserve capacity, and autonomic regulation. Ample clinical and experimental evidence has indicated an emerging role for autophagy, a conservative catabolism process to degrade and recycle cellular organelles and nutrients, in exercise training-offered cardiovascular benefits. Regular physical exercise as a unique form of physiological stress is capable of triggering adaptation while autophagy in particular selective autophagy seems to be permissive to such cardiovascular adaptation. Here in this mini-review, we will summarize the role for autophagy in particular mitochondrial selective autophagy namely mitophagy in the benefit versus risk of physical exercise on cardiovascular function.

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Section: Contemporary Theory Behind Exercise-induced Cardiovasculamentioning

confidence: 99%

“…It is possible that aging or certain metabolic diseases, such as obesity and diabetes, might compromise the regulation of mitophagy during exercise (shown in Figure 1) [58,124]. To examine whether mitophagy response induced by exercise vary in pathological states, a number of studies have been carried out.…”

Section: Mitophagy and Exercisementioning

confidence: 99%

Physical Exercise and Selective Autophagy: Benefit and Risk on Cardiovascular Health

Tian

Chen

et al. 2019

Cells

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“…35 Since autophagy activity also decreases upon aging, aggresome may accumulate in the aged brain. 37,38 The formation of protein aggregate would injury neurons and lead to sustained neuroinflammation in the aged brain. 39,40 The autophagy enhancers can increase the clearance of aggresome and alleviate cognitive impairment in aged brain and neurodegenerative diseases.…”

Section: Discussionmentioning

confidence: 99%

Nicotinamide phosphoribosyltransferase inhibitor ameliorates mouse aging-induced cognitive impairment

Zeng

Wei

Chen

et al. 2021

J Cereb Blood Flow Metab

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Nicotinamide phosphoribosyltransferase (NAMPT) is the key enzyme for the synthesis of nicotinamide adenine dinucleotide (NAD) in the salvaging pathway. Though NAMPT inhibitors such as FK866 were originally developed as anti-cancer drugs, they also display neuroprotective effects. Here we show that the administration of FK866 at 0.5 mg/kg (ip, qod) for four weeks, i.e., ∼1% of the dose used for the treatment of cancer, significantly alleviates the aging-induced impairment of cognition and locomotor activity. Mechanistically, FK866 enhanced autophagy, reduced protein aggregation, and inhibited neuroinflammation indicated by decreasing TNFα, IL-6, GFAP, and Iba1 levels in the aged mouse brain. Though FK866 did not affect the total NAD and nicotinamide mononucleotide (NMN) levels in the mouse brain at the dose we used, FK866 increased nicotinamide (NAM) level in the young mouse brain and decreased NAM level in the aged mouse brain. On the other hand, FK866 did not affect the serum glucose, cholesterol, and triglyceride of young and aged mice and exhibited no effects on the various indices of young mice. Thus, the NAMPT inhibitor can be repurpose to counteract the cognitive impairment upon aging. We also envision that NAMPT inhibitor can be used for the treatment of age-related neurodegenerative diseases.

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“…On the other hand, the alteration of autophagy-mediated by mitochondria (mitophagy) in aged skeletal muscle has been associated with muscle wasting and muscle strength reduction [ 61 , 67 , 68 ]. Mitophagy dysregulation has been denoted as a pathogenic mechanism in muscle atrophy by an increase in LC3-II, p62, and lysosome-associated membrane protein 1 (LAMP1) expression in sarcopenic mice [ 63 ].…”

Section: Aging-related Changes In Skeletal Muscle and Cardiovascular ...mentioning

confidence: 99%

Effect of Physical Activity/Exercise on Oxidative Stress and Inflammation in Muscle and Vascular Aging

Assar

Álvarez‐Bustos

Sosa

et al. 2022

IJMS

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Functional status is considered the main determinant of healthy aging. Impairment in skeletal muscle and the cardiovascular system, two interrelated systems, results in compromised functional status in aging. Increased oxidative stress and inflammation in older subjects constitute the background for skeletal muscle and cardiovascular system alterations. Aged skeletal muscle mass and strength impairment is related to anabolic resistance, mitochondrial dysfunction, increased oxidative stress and inflammation as well as a reduced antioxidant response and myokine profile. Arterial stiffness and endothelial function stand out as the main cardiovascular alterations related to aging, where increased systemic and vascular oxidative stress and inflammation play a key role. Physical activity and exercise training arise as modifiable determinants of functional outcomes in older persons. Exercise enhances antioxidant response, decreases age-related oxidative stress and pro-inflammatory signals, and promotes the activation of anabolic and mitochondrial biogenesis pathways in skeletal muscle. Additionally, exercise improves endothelial function and arterial stiffness by reducing inflammatory and oxidative damage signaling in vascular tissue together with an increase in antioxidant enzymes and nitric oxide availability, globally promoting functional performance and healthy aging. This review focuses on the role of oxidative stress and inflammation in aged musculoskeletal and vascular systems and how physical activity/exercise influences functional status in the elderly.

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Physical exercise, autophagy and cardiometabolic stress in aging

Cited by 7 publications

References 8 publications

Physical Exercise and Selective Autophagy: Benefit and Risk on Cardiovascular Health

Physical Exercise and Selective Autophagy: Benefit and Risk on Cardiovascular Health

Nicotinamide phosphoribosyltransferase inhibitor ameliorates mouse aging-induced cognitive impairment

Effect of Physical Activity/Exercise on Oxidative Stress and Inflammation in Muscle and Vascular Aging

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