Danlou tablet inhibits high-glucose-induced cardiomyocyte apoptosis via the miR-34a-SIRT1 axis

Chen, Rui; Chen, Hongjian; Yang, Zijiang; Zhu, Liang; Bei, Yihua; Chen, Wei; Qiu, Yan

doi:10.1016/j.heliyon.2023.e14479

Cited by 5 publications

(2 citation statements)

References 37 publications

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“…Myocardial fibrosis stands out as a prominent pathological characteristic of DCM, and its regulation involves various miRNAs such as miR-34a, miR-150-5p, miR-18a-5p, miR-30, miR-199 [ 38 ], miR-135b [ 42 ], miR-133a [ 23 ], miR-125b, miR-200b [ 43 ], miR-320 [ 44 ], miR-15a/b [ 45 ], miR-21 [ 46 ], miR-29 [ 47 ] and so on. For instance, research by Bernardo et al [ 48 ] highlighted the involvement of miR-34a in cardiac fibroblasts exposed to high glucose, showing its ability to enhance collagen synthesis through decreasing the level of sirtuin 1 (SIRT1) [ 49 , 50 ]. Che et al [ 51 ] indicated that inhibiting miR-150-5p could ameliorate NF-κB-related inflammation and TGF-β1/Smad-induced cardiac fibrosis through targeting Smad7.…”

Section: Micrornasmentioning

confidence: 99%

Roles of non-coding RNA in diabetic cardiomyopathy

Yao,

Huang,

Chen

et al. 2024

Cardiovasc Diabetol

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In recent years, the incidence of diabetes has been increasing rapidly, posing a serious threat to human health. Diabetic cardiomyopathy (DCM) is characterized by cardiomyocyte hypertrophy, myocardial fibrosis, apoptosis, ventricular remodeling, and cardiac dysfunction in individuals with diabetes, ultimately leading to heart failure and mortality. However, the underlying mechanisms contributing to DCM remain incompletely understood. With advancements in molecular biology technology, accumulating evidence has shown that numerous non-coding RNAs (ncRNAs) crucial roles in the development and progression of DCM. This review aims to summarize recent studies on the involvement of three types of ncRNAs (micro RNA, long ncRNA and circular RNA) in the pathophysiology of DCM, with the goal of providing innovative strategies for the prevention and treatment of DCM.

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Section: Micrornasmentioning

confidence: 99%

Roles of non-coding RNA in diabetic cardiomyopathy

Yao,

Huang,

Chen

et al. 2024

Cardiovasc Diabetol

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“…Neonatal rat CFs were obtained using the tryptic digestion method [27]. Hearts from neonatal Sprague Dawley rats aged 1 to 3 days old were digested with 0.125% trypsin at 4 °C for 6 hours, followed by a 5 minute digestion at 37 °C.…”

Section: Isolation and Culture Of Neonatal Rat Cfsmentioning

confidence: 99%

Salvianolic Acid B (Sal B) ameliorates myocardial fibrosis in diabetic cardiomyopathy through deubiquitinating Smad7

Luo,

Fu,

Wang

et al. 2023

Preprint

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Background Salvianolic acid B (Sal B), a water-soluble phenolic compound derived from Salvia Miltiorrhiza Bunge, is commonly used in Chinese Traditional Medicine for the treatment of cardiovascular diseases. Sal B has shown protecting effects against myocardial fibrosis induced by diabetic cardiomyopathy(DCM) in our previous experiment. This study aimed to investigate the ameliorative effects and potential mechanisms of Sal B in mitigating myocardial fibrosis induced by DCM. Methods In this study, a variety of methods were utilized to investigate the effects of Sal B on improving myocardial fibrosis induced by DCM in vivo and in vitro. These methods included weight measurement, blood glucose analysis, echocardiography, HE staining, Masson's trichrome staining, Sirius red staining, cell proliferation assessment, determination of hydroxyproline levels, immunohistochemical staining, evaluation of fibrosis-associated protein expression (Collagen I, Collagen III, TGF-β1, p-Smad3, Smad3, Smad7, and α-smooth muscle actin), analysis of Smad7 gene expression, and analysis of Smad7 ubiquitin modification. Results The animal test results indicated Sal B could significantly improve cardiac function, inhibit collagen deposition and phenotypic transformation, ameliorate myocardial fibrosis in DCM by up-regulating Smad7, thereby inhibiting TGF-β1 signaling pathway. Additionally, cell experiments demonstrated Sal B could significantly inhibit the proliferation, migration, phenotypic transformation and collagen secretion of cardiac fibroblasts (CFs) induced by high glucose(HG). Sal B could significantly decrease the ubiquitization modifications of Smad7, stabilize the protein expression of Smad7, therefore increase the protein expression of Smad7 in the CFs , inhibit TGF-β1 signaling pathway, that maybe a potential mechanism of Sal B in mitigating myocardial fibrosis induced by DCM. Conclusion In summary, this study revealed that Salvianolic acid B can improve myocardial fibrosis in DCM by deubiquitinating Smad7, stabilizing the protein expression of Smad7, blocking the TGF-β1 signaling pathway.

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