Resveratrol Inhibits Zinc Deficiency-Induced Mitophagy and Exerts Cardiac Cytoprotective Effects

Wang, Pei; Yang, Ying; Guo, Jiabao; Ma, T.; Hu, Yunzi; Huang, Luyao; He, Yonggui; Xi, Jinkun

doi:10.1007/s12011-023-03758-1

Cited by 2 publications

(2 citation statements)

References 43 publications

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“…In addition, resveratrol could improve cardiomyopathy by promoting autophagy/mitophagy in the heart of a Duchenne muscular dystrophy (DMD) model mouse [99]. Resveratrol can protect mitochondria by modulating mitophagy through the alteration of the AMPK signaling pathway in myocardial cells [100]. Furthermore, resveratrol can inhibit hyperglycemia-induced cardiomyocyte hypertrophy by reducing oxidative stress via stimulating mitophagy to keep mitochondrial homeostasis [101].…”

Section: Possible Treatment Tactics With Certain Small Molecules Agai...mentioning

confidence: 99%

“…Resveratrol can protect mitochondria by modulating mitophagy through the alteration of the AMPK signaling pathway in myocardial cells [100]. Furthermore, resveratrol can inhibit hyperglycemia-induced cardiomyocyte hypertrophy by reducing oxidative stress via stimulating mitophagy to keep mitochondrial homeostasis [101].…”

Section: Possible Treatment Tactics With Certain Small Molecules Agai...mentioning

confidence: 99%

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Exogenous and Endogenous Molecules Potentially Proficient to Modulate Mitophagy in Cardiac Disorders

Nakashima,

Suga,

Matsuda

2024

Kinases and Phosphatases

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It has been proposed that procedures which upregulate mitochondrial biogenesis and autophagy by replacing damaged mitochondria with healthy ones may prevent the development of several heart diseases. A member of serine and threonine kinases, adenosine monophosphate-activated protein kinase (AMPK), could play essential roles in the autophagy and/or mitophagy. AMPK is widely distributed in various cells, which might play diverse regulatory roles in different tissues and/or organs. In fact, changes in the kinase function of AMPK due to alteration of activity have been linked with diverse pathologies including cardiac disorders. AMPK can regulate mitochondrial biogenesis via peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) signaling and also improve oxidative mitochondrial metabolism through inhibition of mechanistic/mammalian target of rapamycin (mTOR) pathway, which may also modulate the autophagy/mitophagy through autophagy activating kinase 1 (ULK1) and/or transforming growth factor beta (TGF-β) signaling. Therefore, the modulation of AMPK in autophagy/mitophagy pathway might probably be thought as a therapeutic tactic for several cardiac disorders. As kinases are amongst the most controllable proteins, in general, the design of small molecules targeting kinases might be an eye-catching avenue to modulate cardiac function. Some analyses of the molecular biology underlying mitophagy suggest that nutraceuticals and/or drugs including specific AMPK modulator as well as physical exercise and/or dietary restriction that could modulate AMPK may be useful against several heart diseases. These observations may virtually be limited to preclinical studies. Come to think of these, however, it is speculated that some nutraceutical regimens might have positive potential for managing some of cardiac disorders.

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Section: Possible Treatment Tactics With Certain Small Molecules Agai...mentioning

confidence: 99%

Section: Possible Treatment Tactics With Certain Small Molecules Agai...mentioning

confidence: 99%

Exogenous and Endogenous Molecules Potentially Proficient to Modulate Mitophagy in Cardiac Disorders

Nakashima,

Suga,

Matsuda

2024

Kinases and Phosphatases

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Resveratrol and Vitamin D: Eclectic Molecules Promoting Mitochondrial Health in Sarcopenia

Russo,

Valle,

D’Angeli

et al. 2024

IJMS

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Sarcopenia refers to the progressive loss and atrophy of skeletal muscle function, often associated with aging or secondary to conditions involving systemic inflammation, oxidative stress, and mitochondrial dysfunction. Recent evidence indicates that skeletal muscle function is not only influenced by physical, environmental, and genetic factors but is also significantly impacted by nutritional deficiencies. Natural compounds with antioxidant properties, such as resveratrol and vitamin D, have shown promise in preventing mitochondrial dysfunction in skeletal muscle cells. These antioxidants can slow down muscle atrophy by regulating mitochondrial functions and neuromuscular junctions. This review provides an overview of the molecular mechanisms leading to skeletal muscle atrophy and summarizes recent advances in using resveratrol and vitamin D supplementation for its prevention and treatment. Understanding these molecular mechanisms and implementing combined interventions can optimize treatment outcomes, ensure muscle function recovery, and improve the quality of life for patients.

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Resveratrol Inhibits Zinc Deficiency-Induced Mitophagy and Exerts Cardiac Cytoprotective Effects

Cited by 2 publications

References 43 publications

Exogenous and Endogenous Molecules Potentially Proficient to Modulate Mitophagy in Cardiac Disorders

Exogenous and Endogenous Molecules Potentially Proficient to Modulate Mitophagy in Cardiac Disorders

Resveratrol and Vitamin D: Eclectic Molecules Promoting Mitochondrial Health in Sarcopenia

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