The Relationship between Coronary Artery Disease and SIRT1 Protein

Aşkın, Lütfü; Tıbıllı, Hakan; Tanrıverdi, Okan; Türkmen, Serdar

doi:10.14744/nci.2020.31391

Cited by 16 publications

(10 citation statements)

References 43 publications

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“…Silent information regulator 1 (SIRT1) is a transcriptional regulator with histone deacetylase activity, which can sense the energy status of the body, regulate the expression of other transcription factors, and also participate in the process of regulating cellular metabolic homeostasis [ 32 ]. SIRT1 promotes the deacetylation of lysine residues of PGC-1 α , initiates the transcriptional activity of PGC-1 α , and regulates its expression, which further regulates cellular energy metabolism and mitochondrial biosynthesis and protects cardiomyocytes from oxidative stress [ 33 ]. ATP5D is a subunit of ATP synthase involved in oxidative phosphorylation.…”

Section: Resultsmentioning

confidence: 99%

An Energy Metabolism Study on the Efficacy of Naoxintong Capsules against Myocardial Infarction in a Rat Model

Zhao

Ouyang

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Background. In myocardial ischemia, optimizing the myocardial metabolic phenotype to improve cardiac function is critical. Naoxintong capsules (NXT) are widely prescribed in Chinese medicine for the treatment of cerebrovascular and cardiovascular diseases. Methods. In this study, a rat model of myocardial infarction was established by ligation of the left anterior descending coronary artery. The structure and function of the heart were evaluated using echocardiography. The pathological changes of the rat myocardium and the myocardial volume collagen fraction (CVF) were examined using hematoxylin-eosin (HE) and Masson’s trichrome staining (Masson). The expression of TNF-α and IL-6 were detected by immunohistochemistry. The level of cTnT was also measured to evaluate myocardial injury. In order to study the changes in energy metabolism in myocardial infarction and the effects of NXT, a targeted analysis method for detecting the 29 energy metabolites in cardiac muscle tissue was developed based on UPLC-QQQ-MS. Western blotting was used to detect the expression of proteins related to energy metabolism in myocardia. Results. In the rat model of myocardial infarction, NXT showed obvious effects, such as improving heart function and increasing LVEF and LVFS. HE staining, Masson staining, and immunohistochemical results revealed that NXT decreased inflammatory infiltration, improved myocardial fibrosis, and reduced infarct size. In addition, NXT significantly reduced the level of serum cTnT. The levels of the 29 energy metabolites in cardiac muscle tissue were analyzed using a newly developed targeted analysis method. Compared to the sham group, the levels of 17 metabolites from different energy metabolic pathways, including four compounds in glycolysis metabolism, four compounds in TCA cycle, three compounds in oxidative phosphorylation, four compounds in purine metabolism, and two compounds in glutathione metabolism, displayed obvious changes induced by myocardial ischemia. Expressions of SIRT1, PGC-1α, and ATP5D proteins related to energy metabolism were decreased after myocardial infarction. These perturbations could all be reversed by NXT intervention, suggesting that the therapeutic effects of NXT were partially due to interferences with energy metabolisms. Conclusion. This study provides a useful approach for investigating the mechanism of myocardial infarction and evaluating the efficacy of NXT from energy metabolism.

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Section: Resultsmentioning

confidence: 99%

An Energy Metabolism Study on the Efficacy of Naoxintong Capsules against Myocardial Infarction in a Rat Model

Zhao

Ouyang

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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show abstract

“…Compared with the control group, Bcl-2 expression was reduced, while Bax and cleaved caspase-3 expressions were increased in the LPS group, which were partially reversed by miR-197 inhibitor ( p < 0.01) (Figures 2(d) and 2(e) ). Based on a previous study identifying the pivotal role of SIRT1 in protecting cardiomyocytes from oxidative stress injury [ 24 ], we subsequently determined the expression of SIRT1 in H9c2 cells. Western blot and qRT-PCR revealed that LPS notably downregulated SIRT1 expression, which was reversed via miR-197 inhibition ( p < 0.001) (Figures 3(a) – 3(c) ).…”

Section: Resultsmentioning

confidence: 99%

miR-197 Participates in Lipopolysaccharide-Induced Cardiomyocyte Injury by Modulating SIRT1

Liu

Zhang

Cao

et al. 2022

Cardiology Research and Practice

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Sepsis is a systemic inflammation and is capable of inducing myocarditis, which is a major leading cause of death in patients. Studies have found that miR-197 is correlated with the prognosis of patients with inflammatory heart disease, but its effect on sepsis-induced cardiomyocyte injury remains unclear. We treated H9c2 cells with lipopolysaccharide (LPS), then detected the cell viability via the cell counting kit-8 (CCK-8) assay and quantified miR-197 expression via quantitative real-time polymerase chain reaction (qRT-PCR). Then, we investigated the role of miR-197 in LPS-induced H9c2 cells by CCK-8 assay, flow cytometry, lactate dehydrogenase (LDH) measurement, enzyme-linked immunosorbent assay (ELISA), qRT-PCR, and western blot. Subsequently, silent information regulator 1 (SIRT1) was downregulated in H9c2 cells to explore its interaction with miR-197 under LPS induction. LPS induced miR-197 overexpression in H9c2 cells. LPS restrained viability, the expressions of B-cell lymphoma-2 (Bcl-2) and SIRT1, but promoted apoptosis, LDH release, and levels of interleukin-6 (IL-6), interleukin-1β (IL-1β), acetyl (AC)-p53, BCL2-associated X (Bax), and cleaved caspase-3 in H9c2 cells. miR-197 inhibition reversed the effects of LPS on H9c2 cells. The protective role of miR-197 downregulation in LPS-induced H9c2 cells was reversed by SIRT1 silencing. miR-197 contributed to LPS-induced cardiomyocyte injury by modulating SIRT1, which might be used as a molecular marker in the management of sepsis.

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“…It regulates angiogenesis, and it protects the endothelium against dysfunctional changes and damage to the heart muscle resulting from a reduced perfusion and ischemia. Suppression of the SIRT1 causes monocyte affinity due to endothelial dysfunction [ 53 ]. The gene encoding transcription factor TCF21 has been linked to CAD risk by GWAS in multiple racial/ethnic groups.…”

Section: Coronary Artery Disease and Atherosclerosismentioning

confidence: 99%

Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

et al. 2022

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Cardiovascular diseases (CVDs) are disorders associated with the heart and circulatory system. Atherosclerosis is its major underlying cause. CVDs are chronic and can remain hidden for a long time. Moreover, CVDs are the leading cause of global morbidity and mortality, thus creating a major public health concern. This review summarizes the available information on the pathophysiological implications of CVDs, focusing on coronary artery disease along with atherosclerosis as its major cause and arterial hypertension. We discuss the endothelium dysfunction, inflammatory factors, and oxidation associated with atherosclerosis. Mechanisms such as dysfunction of the endothelium and inflammation, which have been identified as critical pathways for development of coronary artery disease, have become easier to diagnose in recent years. Relatively recently, evidence has been found indicating that interactions of the molecular and cellular elements such as matrix metalloproteinases, elements of the immune system, and oxidative stress are involved in the pathophysiology of arterial hypertension. Many studies have revealed several important inflammatory and genetic risk factors associated with CVDs. However, further investigation is crucial to improve our knowledge of CVDs progression and, more importantly, accelerate basic research to improve our understanding of the mechanism of pathophysiology.

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The Relationship between Coronary Artery Disease and SIRT1 Protein

Cited by 16 publications

References 43 publications

An Energy Metabolism Study on the Efficacy of Naoxintong Capsules against Myocardial Infarction in a Rat Model

An Energy Metabolism Study on the Efficacy of Naoxintong Capsules against Myocardial Infarction in a Rat Model

miR-197 Participates in Lipopolysaccharide-Induced Cardiomyocyte Injury by Modulating SIRT1

Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

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