miR‐34a attenuates myocardial fibrosis in diabetic cardiomyopathy mice via targeting Pin‐1

Zhang, Xiaolong; Zhang, Gang; Bai, Ze-Hong

doi:10.1002/cbin.11512

Cited by 12 publications

(6 citation statements)

References 33 publications

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“…These miR-34a-mediated apoptosis, proliferation and necrosis ultimately contribute to cardiac remodeling (64). Contrary to most studies, a recent report shows that miR-34a ameliorates myocardial fibrosis by reducing type I collagen production, cell viability, and migration and improves cell function in diabetic cardiomyopathy (65). In general, miR-34a inhibition alleviated cardiac and vascular remodeling post ischaemic disease.…”

Section: Mir-34a and Cardiovascular Fibrotic Remodelingmentioning

confidence: 97%

Targeting the microRNA-34a as a Novel Therapeutic Strategy for Cardiovascular Diseases

Hua

Liu

Liang³

et al. 2022

Front. Cardiovasc. Med.

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Cardiovascular diseases (CVDs) are still the main cause of morbidity and mortality worldwide and include a group of disorders varying from vasculature, myocardium, arrhythmias and cardiac development. MicroRNAs (miRs) are endogenous non-coding RNAs with 18–23 nucleotides that regulate gene expression. The miR-34 family, including miR-34a/b/c, plays a vital role in the regulation of myocardial physiology and pathophysiological processes. Recently, miR-34a has been implicated in cardiovascular fibrosis, dysfunction and related cardiovascular disorders as an essential regulator. Interestingly, there is a pivotal link among miR-34a, cardiovascular fibrosis, and Smad4/TGF-β1 signaling. Notably, both loss-of-function and gain-of-function approaches identified the critical roles of miR-34a in cardiovascular apoptosis, autophagy, inflammation, senescence and remodeling by modulating multifunctional signaling pathways. In this article, we focus on the current understanding of miR-34a in biogenesis, its biological effects and its implications for cardiac pathologies including myocardial infarction, heart failure, ischaemia reperfusion injury, cardiomyopathy, atherosclerosis, hypertension and atrial fibrillation. Thus, further understanding of the effects of miR-34a on cardiovascular diseases will aid the development of effective interventions. Targeting for miR-34a has emerged as a potential therapeutic target for cardiovascular dysfunction and related diseases.

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Section: Mir-34a and Cardiovascular Fibrotic Remodelingmentioning

confidence: 97%

Targeting the microRNA-34a as a Novel Therapeutic Strategy for Cardiovascular Diseases

Hua

Liu

Liang³

et al. 2022

Front. Cardiovasc. Med.

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“…RSV has been reported to have antioxidative, anti-inflammatory, antiapoptotic and other effects ( Hu and Li, 2019 ; Yanez et al, 2019 ; Zhang X. L. et al, 2020 ). To clarify the effect of RSV on stem cells, BMSCs were cultured with different concentrations of RSV for different times.…”

Section: Resultsmentioning

confidence: 99%

Resveratrol Pretreatment Improved Heart Recovery Ability of Hyperglycemic Bone Marrow Stem Cells Transplantation in Diabetic Myocardial Infarction by Down-Regulating MicroRNA-34a

Zhang

Wang²,

Gao

et al. 2021

Front. Pharmacol.

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AIM: To examine the effect of resveratrol (RSV) on bone marrow mesenchymal stem cells (BMSCs) under hyperglycemic conditions and on BMSCs transplantation in diabetic rats with myocardial infarction (MI).METHODS:In vitro, BMSCs were isolated from 3-week-old male Sprague Dawley (SD) rats and cultured under hyperglycemic conditions for up to 28 days. Cell viability was analyzed by cell counting kit-8 (CCK-8) assays. The expression of miR-34a was measured by RT-qPCR. Western blotting was used to examine the protein expression of SIRT1, P21, P16, VEGF and HIF-1α. A senescence-associated β-galactosidase assay was used to examine the senescence level of each group. In vivo, a diabetes model was established by feeding rats a high-sugar and high-fat diet for 8 weeks, injecting the animals with streptozotocin (STZ) and continuing high-sugar and high-fat feeding for 4 additional weeks. Then, left anterior descending coronary artery (LAD) cessation was used to established the myocardial infarction (MI) models. Each group of rats was transplanted with differentially preconditioned BMSCs after myocardial infarction. Ultrasound was used to analyze cardiac function 1 and 3 weeks after the operation, and frozen heart sections were used for immunohistochemical analysis, Masson staining and CD31 measurement. In addition, ELISA analysis of serum cytokine levels was performed.RESULTS: This study showed that the viability of BMSCs cultured under hyperglycemic conditions was decreased, the cells became senescent. Besides, an obviously increased in the expression of miR-34a was detected. Moreover, RSV preconditioning reduced the expression of miR-34a in BMSCs after high glucose stimulation and rejuvenated BMSCs under hyperglycemic conditions. Further analysis showed that the transplantation of RSV-BMSCs were benefit to heart recovery following infarction in diabetic rats, promoted proangiogenic factor release and increased arteriole and capillary densities.CONCLUSION: RSV rejuvenated BMSCs after chronic hyperglycemia-induced senescence by interacting with miR-34a and optimized the therapeutic effect of BMSCs on diabetes with myocardial infarction.

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“…In a DCM rat model, the expression of miR-34a was upregulated.While,miR-34a mimic induced H9c2 cell apoptosis in HG condition [25] . Evidence also demonstrated that miR-34a reduced type I collagen production, cell viability, and migration and increased apoptosis of CFs by targeting Pin-1 signaling, so that it could attenuate myocardial fibrosis [26] .…”

Section: Go Enrichment Analysis Of Mrnasmentioning

confidence: 98%

Hub Targets Analysis of miRNA-mRNA-TF Network in Diabetic Cardiomyopathy

Ren¹,

He²,

Miao³

et al. 2021

Preprint

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Background: The pathogenic mechanism and development of the diabetic cardiomyopathy(DCM) has been generally explained, and it is clear that the microRNAs(miRNAs), mRNAs and transcription factors(TFs) participate in the process of the DCM disease. Yet, the hub targets of the disease progression are not clear.Methods: To figure out the problem, we downloaded data sets from the Gene Expression Omnibus(GEO) database (GSE44179 and GSE4745). The targeted mRNAs of miRNAs were downloaded from TargetScan, miRBD and microT-CDS database. Gene Ontology (GO) enrichment of miRNAs and mRNAs were analysed in DAVID.R studio software was used to visualize the results of screened targets and GO enrichment. Cytoscape software was used to visualize the miRNA-mRNA-TF interaction network and calculate the hub targets. Results: We filtered eight miRNAs, nine mRNAs and ten transcription factors(TFs) by bioinformatics analysis, and constructed a miRNA-mRNA-TF network. The top ten degrees of nodes in the network are rno-miR-7a, Hnf4a, rno-miR-17, rno-miR-21, rno-miR-122, rno-miR-200c, Med1, Mlxipl, SP1 and rno-miR-34a, which were closely related to the process of DCM. Conclusion: This study revealed that rno-miR-7a, Hnf4a, rno-miR-17and rno-miR-21 may play vital role in the progress of diabetic cardiomyopathy.

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miR‐34a attenuates myocardial fibrosis in diabetic cardiomyopathy mice via targeting Pin‐1

Cited by 12 publications

References 33 publications

Targeting the microRNA-34a as a Novel Therapeutic Strategy for Cardiovascular Diseases

Targeting the microRNA-34a as a Novel Therapeutic Strategy for Cardiovascular Diseases

Resveratrol Pretreatment Improved Heart Recovery Ability of Hyperglycemic Bone Marrow Stem Cells Transplantation in Diabetic Myocardial Infarction by Down-Regulating MicroRNA-34a

Hub Targets Analysis of miRNA-mRNA-TF Network in Diabetic Cardiomyopathy

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