Daming capsule protects against myocardial infarction by promoting mitophagy via the SIRT1/AMPK signaling pathway

Sun, Xi; Han, Yanna; Dong, Chaorun; Qu, Huan; Yu, Yahan; Ju, Jiaming; Bai, Yunlong; Yang, Baofeng

doi:10.1016/j.biopha.2022.113162

Cited by 7 publications

(4 citation statements)

References 29 publications

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“…And SIRT1 is a cardioprotective molecule that can block cardiomyocyte apoptosis and regulate cardiac energy metabolism 47 . A previous studies showed that Daming capsule facilitates mitophagy by activating the SIRT1/AMPK signaling pathway and inhibiting oxidative stress and inflammatory responses in cardiomyocytes, thereby alleviating myocardial infarction‐induced cardiac dysfunction 48 . Furthermore, knockdown of miR‐217 and miR‐543 attenuates CVB3 infection‐induced cardiomyocyte injury by targeting SIRT1 22 .…”

Section: Discussionmentioning

confidence: 99%

“…47 A previous studies showed that Daming capsule facilitates mitophagy by activating the SIRT1/AMPK signaling pathway and inhibiting oxidative stress and inflammatory responses in cardiomyocytes, thereby alleviating myocardial infarction-induced cardiac dysfunction. 48 Furthermore, knockdown of miR-217 and miR-543 attenuates CVB3 infection-induced cardiomyocyte injury by targeting SIRT1. 22 Our data showed that overexpression of Sema3A in cardiomyocytes significantly increased the protein level of SIRT1.…”

Section: Discussionmentioning

confidence: 99%

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Sema3A alleviates viral myocarditis by modulating SIRT1 to regulate cardiomyocyte mitophagy

Lin

Wei

Zhu

et al. 2023

Environmental Toxicology

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Viral myocarditis (VMC) is a common myocardial inflammatory disease characterized by inflammatory cell infiltration and cardiomyocyte necrosis. Sema3A was reported to reduce cardiac inflammation and improve cardiac function after myocardial infarction, but its role in VMC remains to be explored. Here, a VMC mouse model was established by infection with CVB3, and Sema3A was overexpressed in vivo by intraventricular injection of an adenovirus‐mediated Sema3A expression vector (Ad‐Sema3A). We found that Sema3A overexpression attenuated CVB3‐induced cardiac dysfunction and tissue inflammation. And Sema3A also reduced macrophage accumulation and NLRP3 inflammasome activation in the myocardium of VMC mice. In vitro, LPS was used to stimulate primary splenic macrophages to mimic the macrophage activation state in vivo. Activated macrophages were co‐cultured with primary mouse cardiomyocytes to evaluate macrophage infiltration‐induced cardiomyocyte damage. Ectopic expression of Sema3A in cardiomyocytes effectively protected cardiomyocytes from activated macrophage‐induced inflammation, apoptosis, and ROS accumulation. Mechanistically, cardiomyocyte‐expressed Sema3A mitigated macrophage infiltration‐caused cardiomyocyte dysfunction by promoting cardiomyocyte mitophagy and hindering NLRP3 inflammasome activation. Furthermore, NAM (a SIRT1 inhibitor) reversed the protective effect of Sema3A against activated macrophage‐induced cardiomyocyte dysfunction by suppressing cardiomyocyte mitophagy. In conclusion, Sema3A promoted cardiomyocyte mitophagy and suppressed inflammasome activation by regulating SIRT1, thereby attenuating macrophage infiltration‐induced cardiomyocyte injury in VMC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Sema3A alleviates viral myocarditis by modulating SIRT1 to regulate cardiomyocyte mitophagy

Lin

Wei

Zhu

et al. 2023

Environmental Toxicology

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“…In addition, SIRT1 inhibitors can decrease the protective effect of propofol on renal ischemia-reperfusion-mediated acute lung injury ( 45 ). Moreover, daming capsule, a hypolipidemic drug, promotes mitochondrial autophagy through the SIRT1/AMPK signaling pathway, thereby inhibiting myocardial cell injury and protecting against myocardial infarction ( 46 ). Quercetin has been shown to improve cardiomyocyte susceptibility to hypoxia by regulating SIRT1/TMBIM6-related mitochondrial autophagy and endoplasmic reticulum stress ( 47 ).…”

Section: Discussionmentioning

confidence: 99%

Propofol reduces lipopolysaccharide‑induced cardiomyocyte injury in sepsis by activating SIRT1‑mediated autophagy

Zhou²

2023

Exp Ther Med

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Myocardial injury is an indicator of poor prognosis in sepsis, whereas propofol has been reported to protect the myocardium. Therefore, the present study investigated the effect of propofol on myocardial injury in sepsis and its mechanism. An in vitro model of myocardial cell injury was established in myocardial H9C2 cells using lipopolysaccharide (LPS). The Cell Counting Kit 8 (CCK8) assay was used to investigate the effect of propofol pretreatment on the viability of normal and LPS-challenged H9C2 cells, whereas the lactate dehydrogenase (LDH) detection kit was used to measure the levels of LDH. The expression levels of LC3 were analyzed using an immunofluorescence assay. Western blotting was performed to analyze the expression levels of autophagy-related proteins. Following treatment with the autophagy inhibitor 3-methyladenine, CCK8 assay, TUNEL assay, western blotting, 2,7-dichlorohydrofluorescein diacetate assay and ELISA were performed to investigate whether propofol exerted its effects on cell viability, apoptosis, oxidative stress and inflammation via autophagy. Moreover, to further explore the regulatory mechanism of propofol in myocardial injury, sirtuin 1 (SIRT1) was knocked down via transfection with small interfering RNA, and SIRT1 protein was inhibited via the addition of the SIRT1 inhibitor EX527. The present study demonstrated that propofol activated autophagy in LPS-induced cardiomyocytes, and reversed the effects of LPS on viability, apoptosis, oxidative stress and the inflammatory response. Moreover, SIRT1 knockdown and inhibition decreased the activation of autophagy and the protective effect of propofol on LPS-induced cardiomyocytes. In conclusion, propofol reduced LPS-induced cardiomyocyte injury by activating SIRT1-mediated autophagy.

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“…Berberine promotes autophagy in peritoneal macrophages by activating the nicotinamide adenine dinucleotide (NAD + )/SIRT1/TFEB pathway and inhibiting the PI3K/AKT/mTOR signaling pathway, thereby suppressing macrophage apoptosis [ 34 ]. In a mouse model of myocardial infarction, Tongguan capsule has been demonstrated to promote autophagy by increasing the expression of SIRT1, reducing the phosphorylation of mTOR and its downstream effectors, namely 70 kDa ribosomal protein S6 kinase and 4E binding protein 1, and preventing the inflammation and apoptosis of myocardial cells, thereby improving cardiac remodeling [ 148 ]. Daming capsule has been shown to upregulate the expression of the mitochondrial autophagy receptor nucleotide-binding oligomerization domain-like receptor family member X1 by activating the SIRT1/AMPK signaling pathway, increase mitochondrial autophagy, and inhibit oxidative stress and inflammatory responses in myocardial cells, thereby improving heart function following myocardial infarction [ 149 ].…”

Section: Advances In Sirtuin/autophagy-based Therapiesmentioning

confidence: 99%

The Current State of Research on Sirtuin-Mediated Autophagy in Cardiovascular Diseases

Wang,

Li,

Ding

et al. 2023

JCDD

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Sirtuins belong to the class III histone deacetylases and possess nicotinamide adenine dinucleotide-dependent deacetylase activity. They are involved in the regulation of multiple signaling pathways implicated in cardiovascular diseases. Autophagy is a crucial adaptive cellular response to stress stimuli. Mounting evidence suggests a strong correlation between Sirtuins and autophagy, potentially involving cross-regulation and crosstalk. Sirtuin-mediated autophagy plays a crucial regulatory role in some cardiovascular diseases, including atherosclerosis, ischemia/reperfusion injury, hypertension, heart failure, diabetic cardiomyopathy, and drug-induced myocardial damage. In this context, we summarize the research advancements pertaining to various Sirtuins involved in autophagy and the molecular mechanisms regulating autophagy. We also elucidate the biological function of Sirtuins across diverse cardiovascular diseases and further discuss the development of novel drugs that regulate Sirtuin-mediated autophagy.

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Daming capsule protects against myocardial infarction by promoting mitophagy via the SIRT1/AMPK signaling pathway

Cited by 7 publications

References 29 publications

Sema3A alleviates viral myocarditis by modulating SIRT1 to regulate cardiomyocyte mitophagy

Sema3A alleviates viral myocarditis by modulating SIRT1 to regulate cardiomyocyte mitophagy

Propofol reduces lipopolysaccharide‑induced cardiomyocyte injury in sepsis by activating SIRT1‑mediated autophagy

The Current State of Research on Sirtuin-Mediated Autophagy in Cardiovascular Diseases

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