Aerobic exercise ameliorates myocardial ischemia/reperfusion injury and thrombosis of diabetic rats via activation of AMPK/Sirt1/PGC-1α pathway

Wang, Guandong

doi:10.4149/gpb_2022010

Cited by 11 publications

(5 citation statements)

References 47 publications

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“…These results are sufficient to show that AT promotes cardioprotection and inhibits ERS after MI at least partially through PCAF. Although the mechanism through which AT regulates PCAF is unknown, PCAF interacts with multiple members of the sirtuin deacetylase family 46,47 that are regulated by AT and exert cardioprotective effects in mice with myocardial ischemia, [48][49][50] which may be one of the mechanisms through which PCAF functions. However, the specific mechanism by which AT regulates PCAF and how PCAF affects cardiac remodeling must be further explored in future studies.…”

Section: Discussionmentioning

confidence: 99%

Aerobic training attenuates cardiac remodeling in mice post‐myocardial infarction by inhibiting the p300/CBP‐associated factor

Huang,

Ding,

Shao

et al. 2024

The FASEB Journal

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Aerobic training (AT), an effective form of cardiac rehabilitation, has been shown to be beneficial for cardiac repair and remodeling after myocardial infarction (MI). The p300/CBP‐associated factor (PCAF) is one of the most important lysine acetyltransferases and is involved in various biological processes. However, the role of PCAF in AT and AT‐mediated cardiac remodeling post‐MI has not been determined. Here, we found that the PCAF protein level was significantly increased after MI, while AT blocked the increase in PCAF. AT markedly improved cardiac remodeling in mice after MI by reducing endoplasmic reticulum stress (ERS). In vivo, similar to AT, pharmacological inhibition of PCAF by Embelin improved cardiac recovery and attenuated ERS in MI mice. Furthermore, we observed that both IGF‐1, a simulated exercise environment, and Embelin protected from H2O2‐induced cardiomyocyte injury, while PCAF overexpression by viruses or the sirtuin inhibitor nicotinamide eliminated the protective effect of IGF‐1 in H9C2 cells. Thus, our data indicate that maintaining low PCAF levels plays an essential role in AT‐mediated cardiac protection, and PCAF inhibition represents a promising therapeutic target for attenuating cardiac remodeling after MI.

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Section: Discussionmentioning

confidence: 99%

Aerobic training attenuates cardiac remodeling in mice post‐myocardial infarction by inhibiting the p300/CBP‐associated factor

Huang,

Ding,

Shao

et al. 2024

The FASEB Journal

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“…Upregulation of expression of muscle factor irisin during exercise (treadmill exercise, swimming and sprint training) activates the AMPK signaling pathway [ 51 ]. A previous study has shown that regular exercise activates the AMPK/Sirtuin-1 (SIRT1) pathway, which in turn regulates downstream PGC-1α [ 52 ]. Many other studies have found that exercise delays cognitive decline primarily through the PGC-1α–FNDC5–BDNF signaling pathway in the AD hippocampus [ 53 – 55 ].…”

Section: Methodsmentioning

confidence: 99%

Brain metabolism in Alzheimer’s disease: biological mechanisms of exercise

Liu

Qin

et al. 2023

Transl Neurodegener

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Alzheimer’s disease (AD) is a major subtype of neurodegenerative dementia caused by long-term interactions and accumulation of multiple adverse factors, accompanied by dysregulation of numerous intracellular signaling and molecular pathways in the brain. At the cellular and molecular levels, the neuronal cellular milieu of the AD brain exhibits metabolic abnormalities, compromised bioenergetics, impaired lipid metabolism, and reduced overall metabolic capacity, which lead to abnormal neural network activity and impaired neuroplasticity, thus accelerating the formation of extracellular senile plaques and intracellular neurofibrillary tangles. The current absence of effective pharmacological therapies for AD points to the urgent need to investigate the benefits of non-pharmacological approaches such as physical exercise. Despite the evidence that regular physical activity can improve metabolic dysfunction in the AD state, inhibit different pathophysiological molecular pathways associated with AD, influence the pathological process of AD, and exert a protective effect, there is no clear consensus on the specific biological and molecular mechanisms underlying the advantages of physical exercise. Here, we review how physical exercise improves crucial molecular pathways and biological processes associated with metabolic disorders in AD, including glucose metabolism, lipid metabolism, Aβ metabolism and transport, iron metabolism and tau pathology. How metabolic states influence brain health is also presented. A better knowledge on the neurophysiological mechanisms by which exercise improves AD metabolism can contribute to the development of novel drugs and improvement of non-pharmacological interventions.

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“…It also decreased myocardial injury markers and inflammation responses. The study suggests that aerobic exercise can reduce myocardial ischemia/reperfusion injury and repress thrombosis by activating the AMPK/SIRT1/PGC-1α pathway in rats with T2DM ( Wang, 2022 ). Furthermore, SIRT1 plays a key role in suppressing PPAR-𝛾 in mature adipocytes, decreasing fat accumulation.…”

Section: Sirt1 and Inflammationmentioning

confidence: 98%

SIRT1 and thrombosis

Bettiol,

Urban,

Emmi

et al. 2024

Front. Mol. Biosci.

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Thrombosis is a major cause of morbidity and mortality worldwide, with a complex and multifactorial pathogenesis. Recent studies have shown that SIRT1, a member of the sirtuin family of NAD + -dependent deacetylases, plays a crucial role in regulating thrombosis, modulating key pathways including endothelial activation, platelet aggregation, and coagulation. Furthermore, SIRT1 displays anti-inflammatory activity both in vitro, in vivo and in clinical studies, particularly via the reduction of oxidative stress. On these bases, several studies have investigated the therapeutic potential of targeting SIRT1 for the prevention of thrombosis. This review provides a comprehensive and critical overview of the main preclinical and clinical studies and of the current understanding of the role of SIRT1 in thrombosis.

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Aerobic exercise ameliorates myocardial ischemia/reperfusion injury and thrombosis of diabetic rats via activation of AMPK/Sirt1/PGC-1α pathway

Cited by 11 publications

References 47 publications

Aerobic training attenuates cardiac remodeling in mice post‐myocardial infarction by inhibiting the p300/CBP‐associated factor

Aerobic training attenuates cardiac remodeling in mice post‐myocardial infarction by inhibiting the p300/CBP‐associated factor

Brain metabolism in Alzheimer’s disease: biological mechanisms of exercise

SIRT1 and thrombosis

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