MicroRNA-124a Protects the Myocardium Against Ischemia Reperfusion Injury Through Regulation of the Notch Signaling Pathway

Xu, Weijun; Jiang, Shan; Liu, Qi

doi:10.21470/1678-9741-2020-0357

Cited by 4 publications

(4 citation statements)

References 29 publications

(22 reference statements)

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“…Previous studies investigated whether the Notch signaling-induced proangiogenic effect may be the reason for the beneficial effect after the treatment of MI using traditional Chinese medicine and cell therapy 62,133,[140][141][142][143][144][145] . Many studies have reported that the regulation of non-coding RNAs including miRNAs 123,[146][147][148][149][150][151][152][153][154] , lncRNAs 155,156 , and circRNAs 147 could exert a therapeutic role in myocardial repair. Moreover, some drugs are reported to correlate with the Notch pathway [157][158][159][160][161] .…”

Section: Notch Signaling Pathway In MImentioning

confidence: 99%

Signaling pathways and targeted therapy for myocardial infarction

Zhang

Wang

et al. 2022

Sig Transduct Target Ther

274

117

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Although the treatment of myocardial infarction (MI) has improved considerably, it is still a worldwide disease with high morbidity and high mortality. Whilst there is still a long way to go for discovering ideal treatments, therapeutic strategies committed to cardioprotection and cardiac repair following cardiac ischemia are emerging. Evidence of pathological characteristics in MI illustrates cell signaling pathways that participate in the survival, proliferation, apoptosis, autophagy of cardiomyocytes, endothelial cells, fibroblasts, monocytes, and stem cells. These signaling pathways include the key players in inflammation response, e.g., NLRP3/caspase-1 and TLR4/MyD88/NF-κB; the crucial mediators in oxidative stress and apoptosis, for instance, Notch, Hippo/YAP, RhoA/ROCK, Nrf2/HO-1, and Sonic hedgehog; the controller of myocardial fibrosis such as TGF-β/SMADs and Wnt/β-catenin; and the main regulator of angiogenesis, PI3K/Akt, MAPK, JAK/STAT, Sonic hedgehog, etc. Since signaling pathways play an important role in administering the process of MI, aiming at targeting these aberrant signaling pathways and improving the pathological manifestations in MI is indispensable and promising. Hence, drug therapy, gene therapy, protein therapy, cell therapy, and exosome therapy have been emerging and are known as novel therapies. In this review, we summarize the therapeutic strategies for MI by regulating these associated pathways, which contribute to inhibiting cardiomyocytes death, attenuating inflammation, enhancing angiogenesis, etc. so as to repair and re-functionalize damaged hearts.

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Section: Notch Signaling Pathway In MImentioning

confidence: 99%

Signaling pathways and targeted therapy for myocardial infarction

Zhang

Wang

et al. 2022

Sig Transduct Target Ther

274

117

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“…Accumulated studies have assured the crucial micrornas (mirnas) and their target genes in controlling i/r damage in animal or cell models [ 11 , 12 ]. Meanwhile, mirnas can also influence organ damage after sev treatment via modulating associated pathways.…”

Section: Introductionmentioning

confidence: 99%

Sevoflurane protects against cerebral ischemia/reperfusion injury via microrna-30c-5p modulating homeodomain-interacting protein kinase 1

et al. 2021

Bioengineered

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Sevoflurane (SEV) has been reported to be an effective neuroprotective agent for cerebral ischemia/reperfusion injury (CIRI). However, the precise molecular mechanisms of Sev preconditioning in CIRI remain largely unknown. Therefore, CIRI model was established via middle cerebral artery occlusion method. SEV was applied before modeling. after successful modeling, lentivirus was injected into the lateral ventricle of the brain. Neurological impairment score was performed in each group, and histopathologic condition, infarct volume, apoptosis, inflammation, oxidative stress, microRNA (miR)-30 c-5p and homeodomain-interacting protein kinase 1 (HIPK1) were detected. Mouse hippocampal neuronal cell line HT22 cells were pretreated with SEV, and the in vitro model was stimulated via oxygen-glucose deprivation and reoxygenation. The corresponding plasmids were transfected, and the cell growth was detected, including inflammation and oxidative stress, etc. The targeting of miR-30 c-5p with HIPK1 was examined. The results clarified that reduced miR-30 c-5p and elevated HIPK1 were manifested in CIRI. SEV could improve CIRI and modulate the miR-30 c-5p-HIPK1 axis in vitro and in vivo , and miR-30 c-5p could target HIPK1. Depressed miR-30 c-5p could eliminate the protection of SEV in vitro and in vivo . Repression of HIPK1 reversed the effect of reduced miR-30 c-5p on CIRI. Therefore, it is concluded that SEV is available to depress CIRI via targeting HIPK1 through upregulated miR-30 c-5p.

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“…13,14 For example, miR-21, miR-124 and miR-182-5p were reported to regulate MI/R injury. [15][16][17] The expression of miR-23a-5p was significantly enhanced during myocardial infarction. 18 However, miR-23a-5p has been poorly studied in heart-related diseases.…”

Section: Introductionmentioning

confidence: 99%

“…microRNAs (miRNAs) are members of noncoding RNAs, which play important roles in MI/R injury 13,14 . For example, miR‐21, miR‐124 and miR‐182‐5p were reported to regulate MI/R injury 15–17 . The expression of miR‐23a‐5p was significantly enhanced during myocardial infarction 18 .…”

Section: Introductionmentioning

confidence: 99%

TFAP2C inhibits cell autophagy to alleviate myocardial ischemia/reperfusion injury by regulating miR‐23a‐5p/SFRP5/Wnt5a axis

Zeng

Wei

et al. 2023

The FASEB Journal

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Myocardial ischemia/reperfusion (MI/R) injury contributes to severe injury for cardiomyocytes. In this study, we aimed to explore the underlying mechanism of TFAP2C on cell autophagy in MI/R injury. MTT assay measured cell viability.The cells injury was evaluated by commercial kits. IF detected the level of LC3B.Dual luciferase reporter gene assay, ChIP or RIP assay were performed to verify the interactions between crucial molecules. We found that TFAP2C and SFRP5 expression were decreased while miR-23a-5p and Wnt5a increased in AC16 cells in response to H/R condition. H/R induction led to cell injury and induced autophagy, which were reversed by TFAP2C overexpression or 3-MA treatment (an autophagy inhibitor). Mechanistically, TFAP2C suppressed miR-23a expression through binding to miR-23a promoter, and SFRP5 was a target gene of miR-23a-5p. Moreover, miR-23a-5p overexpression or rapamycin reversed the protective impacts of TFAP2C overexpression on cells injury and autophagy upon H/R condition. In conclusion, TFAP2C inhibited autophagy to improve H/R-induced cells injury by mediating miR-23a-5p/SFRP5/Wnt5a axis.

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MicroRNA-124a Protects the Myocardium Against Ischemia Reperfusion Injury Through Regulation of the Notch Signaling Pathway

Cited by 4 publications

References 29 publications

Signaling pathways and targeted therapy for myocardial infarction

Signaling pathways and targeted therapy for myocardial infarction

Sevoflurane protects against cerebral ischemia/reperfusion injury via microrna-30c-5p modulating homeodomain-interacting protein kinase 1

TFAP2C inhibits cell autophagy to alleviate myocardial ischemia/reperfusion injury by regulating miR‐23a‐5p/SFRP5/Wnt5a axis

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