Non-coding RNAs modulate autophagy in myocardial ischemia-reperfusion injury: a systematic review

Huang, Fuwen; Mai, Jing-Ting; Chen, Jingwei; He, Yinying; Chen, Xiaojun

doi:10.1186/s13019-021-01524-9

Cited by 9 publications

(11 citation statements)

References 87 publications

(85 reference statements)

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“…It has been reported that the pathogenesis of MIRI is closely related to ncRNAs, including miRNAs, long noncoding RNAs, and circular RNAs. 46 , 47 , 48 In the present study, by analyzing existing MIRI‐related miRNAs sequencing results from the GEO database, bioinformatics analysis revealed differential expression miRNAs in MIRI, including miR‐582‐5p, let‐7f‐1‐3p, miR‐714, miR‐23b‐5p, miR‐706, miR‐1940, and miR‐7030‐5p. Then, establishing HL‐1 cell models in vitro and mouse animal models in vivo, the results showed that miR‐582‐5p was significantly increased in cardiomyocytes after H/R.…”

Section: Discussionmentioning

confidence: 72%

“…It has been reported that the pathogenesis of MIRI is closely related to ncRNAs, including miRNAs, long noncoding RNAs, and circular RNAs. [47][48][49] In the present study, by analyzing existing MIRI-related miRNAs sequencing results from the GEO database, bioinformatics analysis revealed differential expression miRNAs in MIRI, including miR-582-5p, let-7f-1-3p, miR-714, miR-23b-5p, miR-706, miR-1940, and miR-7030-5p. Then, establishing HL-1 cell models in vitro and mouse animal models in vivo, the results showed that miR-582-5p was significantly increased in cardiomyocytes after H/R.…”

Section: Discussionmentioning

confidence: 79%

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MicroRNA‐582‐5p targeting Creb1 modulates apoptosis in cardiomyocytes hypoxia/reperfusion‐induced injury

Niu

Wang

Yang

et al. 2022

Immunity Inflam & Disease

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Background Myocardial ischemia–reperfusion injury (MIRI) caused by the reperfusion therapy of myocardial ischemic diseases is a kind of major disease that threatens human health and lives severely. There are lacking of effective therapeutic measures for MIRI. MicroRNAs (miRNAs) are abundant in mammalian species and play a critical role in the initiation, promotion, and progression of MIRI. However, the biological role and molecular mechanism of miRNAs in MIRI are not entirely clear. Methods We used bioinformatics analysis to uncover the significantly different miRNA by analyzing transcriptome sequencing data from myocardial tissue in the mouse MIRI model. Multiple miRNA‐related databases, including miRdb, PicTar, and TargetScan were used to forecast the downstream target genes of the differentially expressed miRNA. Then, the experimental models, including male C57BL/6J mice and HL‐1 cell line, were used for subsequent experiments including quantitative real‐time polymerase chain reaction analysis, western blot analysis, hematoxylin and eosin staining, flow cytometry, luciferase assay, gene interference, and overexpression. Results MiR‐582‐5p was found to be differentially upregulated from the transcriptome sequencing data. The elevated levels of miR‐582‐5p were verified in MIRI mice and hypoxia/reperfusion (H/R)‐induced HL‐1 cells. Functional experiments revealed that miR‐582‐5p promoted apoptosis of H/R‐induced HL‐1 cells via downregulating cAMP‐response element‐binding protein 1 (Creb1). The inhibiting action of miR‐582‐5p inhibitor on H/R‐induced apoptosis was partially reversed after Creb1 interference. Conclusions Collectively, the research findings reported that upregulation of miR‐582‐5p promoted H/R‐induced cardiomyocyte apoptosis by inhibiting Creb1. The potential diagnostic and therapeutic strategies targeting miR‐582‐5p and Creb1 could be beneficial for the MIRI treatment.

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Section: Discussionmentioning

confidence: 72%

Section: Discussionmentioning

confidence: 79%

MicroRNA‐582‐5p targeting Creb1 modulates apoptosis in cardiomyocytes hypoxia/reperfusion‐induced injury

Niu

Wang

Yang

et al. 2022

Immunity Inflam & Disease

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“…The hypomethylation in ATG7 promoter might enhance ATG7 expression in CHD. The up-regulated ATG7 catalyzed the formation of LC3-II by collaborating with LC3-I, ATG3 and phosphatidyl ethanolamine (PE) [ 20 , 21 ]. The increased LC3-II facilitated the phagophore elongation [ 22 ], which might lead to monocyte dysfunction through aberrant excessive autophagy.…”

Section: Discussionmentioning

confidence: 99%

“…CHD patients and controls were marked in yellow and green, respectively. The trendline of all individuals was marked in red ethanolamine (PE) [20,21]. The increased LC3-II facilitated the phagophore elongation [22], which might lead to monocyte dysfunction through aberrant excessive autophagy.…”

Section: Discussionmentioning

confidence: 99%

Identification of DNA methylation-regulated genes as potential biomarkers for coronary heart disease via machine learning in the Framingham Heart Study

Zhang

Wang

et al. 2022

Clin Epigenet

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Background DNA methylation-regulated genes have been demonstrated as the crucial participants in the occurrence of coronary heart disease (CHD). The machine learning based on DNA methylation-regulated genes has tremendous potential for mining non-invasive predictive biomarkers and exploring underlying new mechanisms of CHD. Results First, the 2085 age-gender-matched individuals in Framingham Heart Study (FHS) were randomly divided into training set and validation set. We then integrated methylome and transcriptome data of peripheral blood leukocytes (PBLs) from the training set to probe into the methylation and expression patterns of CHD-related genes. A total of five hub DNA methylation-regulated genes were identified in CHD through dimensionality reduction, including ATG7, BACH2, CDKN1B, DHCR24 and MPO. Subsequently, methylation and expression features of the hub DNA methylation-regulated genes were used to construct machine learning models for CHD prediction by LightGBM, XGBoost and Random Forest. The optimal model established by LightGBM exhibited favorable predictive capacity, whose AUC, sensitivity, and specificity were 0.834, 0.672, 0.864 in the validation set, respectively. Furthermore, the methylation and expression statuses of the hub genes were verified in monocytes using methylation microarray and transcriptome sequencing. The methylation statuses of ATG7, DHCR24 and MPO and the expression statuses of ATG7, BACH2 and DHCR24 in monocytes of our study population were consistent with those in PBLs from FHS. Conclusions We identified five DNA methylation-regulated genes based on a predictive model for CHD using machine learning, which may clue the new epigenetic mechanism for CHD.

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“…For instance, downregulation of miR-1, miR-let-7f, and miR-124 was observed in the cerebral cortex and hippocampus of mice following I/R [ 12 – 14 ]. Many studies have also shown that miRNA contributing to myocardial I/R injury, such as miR-204, miR-30e, and miR-221, was abnormally expressed in the myocardium and found to play a regulatory role in myocardial I/R injury by modulating autophagy [ 15 ]. Therefore, identification of I/R-associated miRNAs is important as it could provide new ideas for the treatment of myocardial I/R injury.…”

Section: Introductionmentioning

confidence: 99%

Ischemic Postconditioning Protects against Aged Myocardial Ischemia/Reperfusion Injury by Transcriptional and Epigenetic Regulation of miR-181a-2-3p

Ding

Xiong

et al. 2022

Oxidative Medicine and Cellular Longevity

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Ischemic postconditioning (IPostC) has been proposed as a strategy to mitigate the risk of ischemia/reperfusion (I/R) injury, and autophagy is involved in I/R-induced aged myocardial injury, while the underlying mechanism of IPostC-regulated autophagy is unknown. Here, we implemented miRNA sequencing analysis in aged cardiomyocytes to identify a novel miR-181a-2-3p after HPostC, which inhibits autophagy by targeting AMBRA1 in aged myocardium to protect I/R-induced aged myocardial injury. Mechanistically, we identified that IPostC can induce DNA hypomethylation and H3K14 hyperacetylation of miR-181a-2-3p promoter due to the decreased binding of DNMT3b and HDAC2 at its promoter, which contributes to enhancing the expression of miR-181a-2-3p. More importantly, cooperation of DNMT3b and HDAC2 inhibits the binding of c-Myc at the miR-181a-2-3p promoter in aged cardiomyocytes. In summary, IPostC attenuates I/R-induced aged myocardial injury through upregulating miR-181a-2-3p expression, which is an attribute to transcriptional and epigenetic regulation of its promoter. Our data indicate that miR-181a-2-3p may be a potential therapeutic target against I/R injury in aged myocardium.

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Non-coding RNAs modulate autophagy in myocardial ischemia-reperfusion injury: a systematic review

Cited by 9 publications

References 87 publications

MicroRNA‐582‐5p targeting Creb1 modulates apoptosis in cardiomyocytes hypoxia/reperfusion‐induced injury

MicroRNA‐582‐5p targeting Creb1 modulates apoptosis in cardiomyocytes hypoxia/reperfusion‐induced injury

Identification of DNA methylation-regulated genes as potential biomarkers for coronary heart disease via machine learning in the Framingham Heart Study

Ischemic Postconditioning Protects against Aged Myocardial Ischemia/Reperfusion Injury by Transcriptional and Epigenetic Regulation of miR-181a-2-3p

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