Mitochondrial biogenesis and apoptosis as underlying mechanisms involved in the cardioprotective effects of Gallic acid against D-galactose-induced aging

Zarei, Mohammad; Sarihi, Abdolrahman; Zamani, Alireza; Raoufi, Safoura; Karimi, Seyed Asaad; Ramezani-Aliakbari, Fatemeh

doi:10.1007/s11033-023-08670-4

Cited by 8 publications

(2 citation statements)

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“…Mitochondrial biogenesis is characterized by generating new mitochondria and increasing mitochondrial content and number. Alterations in the mitochondria fusion and fission processes as well as mitophagy suppression might lead to a decrease in mitochondrial biogenesis ( 141 ). PGC1-α is a vital transcriptional regulator of mitochondrial biogenesis and can activate the transcriptional expression of nuclear respiratory factor-1/2 (NRF-1/2).…”

Section: Discussionmentioning

confidence: 99%

“…Acting as an upstream factor, SIRT1 directly stimulated PGC1-α expression ( 145 , 146 ). Zarei et al observed that stimulating the SIRT1/PGC1-α pathway reduced the cardiomyocytes toxicity of D-galactose-induced by improving mitochondrial biogenesis ( 141 ). According to Santos-Gallego et al, Empagliflozin therapy enhanced heart function and mitochondria energetics in porcine model of HF, which was achieved by upregulating the expression of AMPK and PGC-1α ( 15 ).…”

Section: Discussionmentioning

confidence: 99%

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The changes of cardiac energy metabolism with sodium-glucose transporter 2 inhibitor therapy

Su,

Ji,

et al. 2023

Front. Cardiovasc. Med.

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Background/aimsTo investigate the specific effects of s odium-glucose transporter 2 inhibitor (SGLT2i) on cardiac energy metabolism.MethodsA systematic literature search was conducted in eight databases. The retrieved studies were screened according to the inclusion and exclusion criteria, and relevant information was extracted according to the purpose of the study. Two researchers independently screened the studies, extracted information, and assessed article quality.ResultsThe results of the 34 included studies (including 10 clinical and 24 animal studies) showed that SGLT2i inhibited cardiac glucose uptake and glycolysis, but promoted fatty acid (FA) metabolism in most disease states. SGLT2i upregulated ketone metabolism, improved the structure and functions of myocardial mitochondria, alleviated oxidative stress of cardiomyocytes in all literatures. SGLT2i increased cardiac glucose oxidation in diabetes mellitus (DM) and cardiac FA metabolism in heart failure (HF). However, the regulatory effects of SGLT2i on cardiac FA metabolism in DM and cardiac glucose oxidation in HF varied with disease types, stages, and intervention duration of SGLT2i.ConclusionSGLT2i improved the efficiency of cardiac energy production by regulating FA, glucose and ketone metabolism, improving mitochondria structure and functions, and decreasing oxidative stress of cardiomyocytes under pathological conditions. Thus, SGLT2i is deemed to exert a benign regulatory effect on cardiac metabolic disorders in various diseases.Systematic review registrationhttps://www.crd.york.ac.uk/, PROSPERO (CRD42023484295).

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Section: Discussionmentioning

confidence: 99%