MiRNA-122-5p inhibitor abolishes angiotensin II–mediated loss of autophagy and promotion of apoptosis in rat cardiofibroblasts by modulation of the apelin-AMPK-mTOR signaling

Yang, Mei; Song, Juanjuan; Yang, Xinchun; Zhong, Guangzhen; Zhong, Jiu-Chang

doi:10.1007/s11626-022-00651-4

Cited by 14 publications

(7 citation statements)

References 32 publications

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“…Current studies have found that miRNA‐122 increases the levels of fibrotic factors such as collagen 1α1, collagen 1α2 and transforming growth factorβ1 (TGFβ1) in non‐alcoholic fatty liver disease cell models, thereby increasing the occurrence of fibrosis 22,23 . Administration of miRNA‐122 inhibitors reduces TGFβ‐induced key fibrotic signalling pathways, promotes collagen synthesis and stimulates fibrin production, leading to the accumulation of fibroblasts and extracellular matrix (ECM) in hypertension and cardiovascular disease 24,25 …”

Section: Regulating Autophagymentioning

confidence: 99%

“…22,23 Administration of miRNA-122 inhibitors reduces TGFβ-induced key fibrotic signalling pathways, promotes collagen synthesis and stimulates fibrin production, leading to the accumulation of fibroblasts and extracellular matrix (ECM) in hypertension and cardiovascular disease. 24,25 Li et al showed that MSC treatment improved damaged kidney structure and reduced RF by inhibiting autophagy and interfering with the mammalian target of rapamycin (mTOR) signalling pathway. The authors determined that these effects were due to excreted exosomes mainly containing miRNA-122.…”

Section: Regulating Autophagymentioning

confidence: 99%

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Mesenchymal stem cell‐derived extracellular vesicles in treatment against renal fibrosis

Wang,

Cui,

et al. 2023

Clinical and Translational Dis

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BackgroundRenal fibrosis (RF) is the main pathological pathway of acute kidney injury and chronic kidney disease. Its main pathological feature is extracellular matrix aggregation in the renal stroma and glomerulus. There is currently no effective treatment to delay or treat RF. Mesenchymal stem cells (MSCs) are multipotent somatic stem cells that can direct differentiation, direct cell‐cell interactions and have secretory activity. The most important secretory activity of MSCs is mediated by extracellular vesicles (EVs). At present, there is increasing evidence that EVs produced by MSCs may be used in regenerative methods of tissue repair.AimThe goal of this review is to present the latest efficacy of MSC‐EVs in the prevention, treatment and improvement of RF caused by acute and chronic kidney injury and reveals the molecular mechanism of MSCs in various models.Results and discussionMSC‐EVs show potential for RF by regulating autophagy, inhibiting apoptosis, countering oxidation, suppressing inflammation, reducing EMT and modulating angiogenesis.ConclusionMSC‐EVs show potential for treating RF. However, more studies establishing their safety, efficiency and specific mechanisms in the context of RF are still needed before further clinical application.

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Section: Regulating Autophagymentioning

confidence: 99%

Section: Regulating Autophagymentioning

confidence: 99%

Mesenchymal stem cell‐derived extracellular vesicles in treatment against renal fibrosis

Wang,

Cui,

et al. 2023

Clinical and Translational Dis

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“…In addition, miR-224, miR-765, and miR-195 inhibit apelin expression [213][214][215]. Recent studies have demonstrated that miR-122-5P negatively regulates autophagy, apoptosis, and oxidative stress in rat cardiac fibroblasts by regulating the apelin-AMPK-mTOR signaling pathway [216], and miR-122-5p can also promote tumorigenesis and cardiac remodeling in hypertensive rats by regulating the ELABELA/apelin-apelin receptor axis and angiotensin-converting enzyme 2 (ACE2)-growth differentiation factor 15 (GDF15)-porimin signaling pathways [21].…”

Section: Exercise Modulates Myokine Expression Via Epigenetic Regulationmentioning

confidence: 99%

Impact of Exercise and Aging on Mitochondrial Homeostasis in Skeletal Muscle: Roles of ROS and Epigenetics

Wang

et al. 2022

Cells

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Aging causes degenerative changes such as epigenetic changes and mitochondrial dysfunction in skeletal muscle. Exercise can upregulate muscle mitochondrial homeostasis and enhance antioxidant capacity and represents an effective treatment to prevent muscle aging. Epigenetic changes such as DNA methylation, histone posttranslational modifications, and microRNA expression are involved in the regulation of exercise-induced adaptive changes in muscle mitochondria. Reactive oxygen species (ROS) play an important role in signaling molecules in exercise-induced muscle mitochondrial health benefits, and strong evidence emphasizes that exercise-induced ROS can regulate gene expression via epigenetic mechanisms. The majority of mitochondrial proteins are imported into mitochondria from the cytosol, so mitochondrial homeostasis is regulated by nuclear epigenetic mechanisms. Exercise can reverse aging-induced changes in myokine expression by modulating epigenetic mechanisms. In this review, we provide an overview of the role of exercise-generated ROS in the regulation of mitochondrial homeostasis mediated by epigenetic mechanisms. In addition, the potential epigenetic mechanisms involved in exercise-induced myokine expression are reviewed.

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“…Therefore, apelin-13 may enhance the cardio-protective effect of heart under K 2 Cr 2 O 7 -induced pathological states, which may be regulated by the MAPK and PI3K/Akt signaling pathways. Apelin-13, as a ligand, is widely involved in regulating the cardiovascular process because of its strong biological activity of peptide hormone, and it can promote the inner walls of blood vessels and tube formation of microvascular endothelial cells and regulate the blood pressure and myocardial injury [5]. However, the protective effects and the underlying mechanism of apelin-13 against Cr (VI)-induced heart injury remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Apelin-13 Alleviates Hexavalent Chromium-Induced Myocardial Injury by Inhibiting ROS-mediated Oxidative Damage and Regulating Multiple Signals

Zhang

Liu³

et al. 2022

Preprint

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Background Hexavalent chromium (Cr (VI)) from environmental pollution shows severe toxicity towards human organs by causing oxidative damage. Apelin-13 may inhibit oxidative damage by blocking ROS accumulation and regulating multiple signals. Methods However, whether apelin-13 can attenuate Cr (VI)-induced toxicity has not been explored. Herein, the protective effect and molecular mechanism of apelin-13 against K2Cr2O7-induced cardiotoxicity in vitro and in vivo were evaluated. Results Apelin-13 significantly inhibited K2Cr2O7-induced H9c2 cytotoxicity and apoptosis, followed by the attenuated PARP cleavage and caspase activation. Further investigation revealed that apelin-13 co-treatment effectively suppressed K2Cr2O7-induced oxidative damage by inhibiting ROS accumulation. Moreover, apelin-13 co-treatment dramatically normalized MAPKs and PI3K/AKT pathways in K2Cr2O7-treated H9c2 cells. Importantly, apelin-13 administration in vivo effectively attenuated myocardial fibrosis, improved angiogenesis, and inhibited myocardial abnormal proliferation and apoptosis. Conclusions Ultimately, it alleviated K2Cr2O7-induced myocardial injury in rats.Taken together, our findings validated the strategy of the use of apelin-13 to effectively combat Cr (VI)-induced myocardial injury.

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MiRNA-122-5p inhibitor abolishes angiotensin II–mediated loss of autophagy and promotion of apoptosis in rat cardiofibroblasts by modulation of the apelin-AMPK-mTOR signaling

Cited by 14 publications

References 32 publications

Mesenchymal stem cell‐derived extracellular vesicles in treatment against renal fibrosis

Mesenchymal stem cell‐derived extracellular vesicles in treatment against renal fibrosis

Impact of Exercise and Aging on Mitochondrial Homeostasis in Skeletal Muscle: Roles of ROS and Epigenetics

Apelin-13 Alleviates Hexavalent Chromium-Induced Myocardial Injury by Inhibiting ROS-mediated Oxidative Damage and Regulating Multiple Signals

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