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OBJECTIVES@#This study aims to construct endogenous exosomes abundantly loaded with miR-1 and investigate the role of exosome-mediated microRNA-1 (miR-1) delivery on CAL-27 cell proliferation.@*METHODS@#Exosomes secreted by miR-1-overexpressing HEK293 cells (miR1-EXO) were purified via ultracentrifugation and subjected to transmission electron microscopy, nanoparticle analysis, Western blot analysis, and quantitative polymerase chain reaction (qPCR). CAL-27 cells were cocultured with exosomes secreted by HEK293 cells (CON-EXO) and miR1-EXO and equivalent phosphate buffer saline. The intracellular transport of exosomes was measured by using immunofluorescence, the expression of miR-1 and its target gene MET were investigated via qPCR, CAL-27 cell proliferation was measured through MTT assay, and cell cycle state was determined by applying flow cytometry.@*RESULTS@#Electron microscopy revealed that miR1-EXO and CON-EXO were spherical or cup-shaped with an average diameter of approximately 110 nm. The well-known exosome markers CD9, Tsg101, and Alix were enriched. The expression of miR-1 in miR1-EXO was higher than that in CON-EXO (285.80±14.33 vs 1.00±0.06, @*CONCLUSIONS@#Exosomes secreted from miR1-EXO cells could load abundant miR-1. Exosomal miR-1 delivered into CAL-27 cells by using miR1-EXO suppressed the expression of MET mRNA and inhibited cell proliferation.
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Humans , Cell Cycle , Cell Proliferation , Exosomes , HEK293 Cells , MicroRNAsABSTRACT
Objective:To evaluate the diagnostic value of circulating microRNA-1 (miR-1) in early coronary artery plaque rupture in patients with stable coronary artery disease (SCAD).Methods:A prospective cohort study was conducted. Sixty-seven patients with SCAD admitted to the department of cardiology of the Third Affiliated Hospital of Soochow University from January to June in 2019 were enrolled. All patients had completed coronary angiography (CAG), percutaneous coronary intervention (PCI) single stent implantation or only CAG was performed according to the CAG results. Blood samples were collected before (0 hour) and 3 hours after the procedure. The expression of plasma miR-1 was detected by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR), and electrocardiogram was used to detect cardiac troponin I (cTnI) levels. The difference of miR-1 and cTnI levels in PCI or CAG patients before and after procedure were compared, and the value for early diagnosis of coronary artery plaque rupture in SCAD patients was evaluated. The diagnostic efficacy was evaluated by the receiver operating characteristic curve (ROC curve).Results:There were 38 CAG patients and 29 PCI patients. There were no significant differences in gender, age, previous history (without hypertension history) and baseline data of cardiac function between the two groups. The expression of miR-1 after PCI was significantly higher than that before PCI [2 -ΔΔCt: 2.11 (1.56, 2.73) vs. 1.26 (1.07, 1.92), P < 0.01], and there was no significant difference in cTnI level before and after PCI [μg/L: 0.00 (0.00, 0.02) vs. 0.00 (0.00, 0.02), P > 0.05]. There were no significant differences in miR-1 and cTnI levels before and after procedure in the CAG group [miR-1 (2 -ΔΔCt): 1.09 (1.00, 1.40) vs. 1.21 (1.00, 1.71), cTnI (μg/L): 0.00 (0.00, 0.02) vs. 0.00 (0.00, 0.02), both P > 0.05]. ROC curve analysis showed that the area under ROC curve (AUC) and 95% confidence interval (95% CI) of miR-1 in the diagnosis of coronary plaque rupture were 0.794 (0.687-0.900), P < 0.01, the sensitivity was 82.8%, the specificity was 68.4%, and the optimal cut-off value was 1.51. The AUC and 95% CI of the difference of miR-1 before and after operation (ΔmiR-1) were 0.704 (0.567-0.842), P = 0.004, the sensitivity was 62.1%, the specificity was 84.2%, and the optimal cut-off value was 0.39. The efficancy of miR-1 and ΔmiR-1 after procedure to diagnose coronary plaque rupture in patients with SCAD was similar ( Z = 1.287, P = 0.198). However, baseline miR-1 might not predict whether patients with SCAD need PCI or not (AUC = 0.630, P > 0.05). Multivariate binary Logistic regression analysis showed that increased postoperative miR-1 expression was an independent risk factor for coronary plaque rupture in SCAD patients [odds ratios ( OR) = 2.887, 95% CI was 1.044-7.978, P = 0.041]. Conclusion:Circulating miR-1 might have the value for early diagnosis of coronary artery plaque rupture in SCAD patients.
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ObjectivecircRNAs play an important role in tumor development, but the relationship between circRNAs and hepatocellular carcinoma remains to be further explored. The present study aimed to bioinformatically analyze the target gene of microRNA-1. Another aim was to screen circRNAs that are associated with target genes and differentially expressed in hepatocellular carcinoma cells, as well as provide theoretical basis for clinical screening of molecular markers and targeted therapies related to hepatocellular carcinoma.MethodsThe miRNA related database used for the prediction of microRNA-1 target genes, and the bioinformatic analysis of the target genes of microRNA-1 involved functional enrichment analysis and signal transduction pathway enrichment. Then, the circRNAs, which are related to the downstream target genes of microRNA-1, are screened through the circRNA database.ResultsThe number of microRNA-1 target genes was 230 in miRNA related database. Through GO analysis, it was found that the target genes of microRNA-1 had a strong tendency in regulation, and were mainly enriched in three aspects: biological function, biological process and cell localization.The target genes of microRNA-1 are involved in the function of proteins, regulation of biosynthesis, cofactor binding, enzyme regulation and other biological processes. Predicted target genes of miRNA-1 were significantly enriched in cancer signaling pathways, hepatitis B occurrence, endocytosis and splicing pathways. Further, 21 circRNAs related to the target gene of microRNA-1 were found in three circRNA databases, wherein hsa_circ_0004651 was highly expressed in hepatocellular carcinoma cell line HepG2 and its pavent gene was hnRNPD.ConclusionMicroRNA-1 influence the occurrence of hepatocellular carcinoma development through the regulation of protein and enzyme. Hsa_circ_0004651 may affect the development of hepatocellular carcinoma with microRNA-1 and its parental gene hnRNPD.
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@#Objective To systematically evaluate the clinical value of miRNA-1 in the diagnosis of acute myocardial infarction (AMI) patients. Methods We searched PubMed, EMbase, Cochrane Library, CNKI, Wangfang, VIP, etc databases to identify literature about miRNA-1 in the diagnosis of AMI. Quality of the included literature was assessed by (quality assessment for diagnostic accuracy studies-2, QUADAS-2). The indices of pooled sensitivity (Sen), specificity (Spe), positivity likelihood ratio (PLR), negative likelihood ratio (NLR), diagnosis odds ratio (DOR), and the area under the summary receiver operating characteristic (SROC) curve were pooled using MetaDisc 1.4 software. Results A total of 12 articles were included. According to the different populations of miRNA-1 to be tested, subgroup analysis of healthy people (7 articles) and non-AMI disease groups (5 articles) was conducted. The results showed that AMI compared with healthy people, the pooled Sen was 0.78 with 95%CI 0.73 to 0.82, Spe was 0.88 with 95%CI 0.83 to 0.91 of miRNA-1 in the diagnosis of AMI. AUC of SROC curve was 0.911 2. Comparison of AMI and non-AMI patients, the pooled Sen was 0.59 with 95%CI 0.54 to 0.64, Spe was 0.74 with 95%CI 0.68 to 0.79 of miRNA-1 in the diagnosis of AMI. AUC of SROC curve was 0.743 2. Conclusion MiRNA-1 has a certain value in the diagnosis of AMI. It has an advantage in identifying AMI and patients with other systemic diseases, and can be combined with other biomarkers to diagnose AMI.
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Objective: To study the effect of picroside Ⅱ on the expression of microRNA-1 (miR-1) in the H2O2-induced H9c2 cardiomyocytes damage, in order to explore the mechanism of picroside Ⅱ in protecting H9c2 cardiomyocytes from oxidative stress. Method: H9c2 cardiomyocytes were divided into 6 groups:control group, model group (H2O2 200 μmol·L-1), picroside Ⅱ (50, 100, 200 μmol·L-1)+H2O2 (200 μmol·L-1) group and picroside Ⅱ (200 μmol·L-1) group. Picroside Ⅱ group was incubated with picroside Ⅱ for 6 h and then cultured with H2O2 for 2 h. At the end of drugs treatment, the cell viability and the cellular damage of cardiomyocytes were respectively assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) and lactate dehydrogenase (LDH) assays. 4',6-diamidino-2-phenylindole (DAPI) staining and cysteinyl aspartate specific proteinase-3 (Caspase-3) test were used to evaluate cell apoptosis. The mRNA expressions of Caspase-3,B-cell lymphoma-2 (Bcl-2) and miR-1 were measured by Real-time polymerase chain reaction (Real-time PCR). The protein expression of Bcl-2 was detected by Western blot. Result:Compared with the control group, H2O2 could significantly decrease the cell viability and increase the rate of apoptosis, up-regulate mRNA expression of Caspase-3 and miR-1, and down-regulate expression of Bcl-2 in H9c2 cells (PPPPPPPConclusion:Picroside Ⅱ has a protective effect on H9c2 cells from H2O2-induced cardiomyocyte injury by down-regulating mRNA-1 expression and up-regulating the expression of the downstream Bcl-2.
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Objective: To investigate the inhibitory effect of leonurine on cardiomyocyte hypertrophy induced by angiotensin Ⅱ(Ang Ⅱ) and its effect on p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway and miRNA-1.Method: Cardiomyocyte hypertrophy was induced by Ang Ⅱ (0.1 μmol·L-1) in primary neonatal cardiomyocytes. Experiments were designed in 6 groups as following:normal group, model group, p38 MAPK inhibitor group (SB203580, 10 μmol·L-1), low-dose(5 μmol·L-1), middle-dose(10 μmol·L-1) and high-dose(20 μmol·L-1) group. The cardiomyocyte surface area was measured by image software, and the protein contents were detected by Lowry. The concentrations of ANP in the culture supernatant were measured by enzyme-linked immunosorbent assay (ELISA). The expression level of miRNA-1 was detected by Real-time fluorescence quantitative polymerase chain reaction (Real-time PCR), and the protein expression levels of endothelin-1 (ET-1), p38 MAPK, p-p38 MAPK, myocyte enhancer factor 2 (MEF2), β-myosin heavy chain (β-MHC), α-myosin heavy chain (α-MHC) were detected by Western blot.Result: Compared with normal group, the surface area of cardiomyocyte, the protein contents, the concentrations of ANP, and the protein expression levels of ET-1, p38 MAPK, p-p38 MAPK, MEF2, β-MHC in model group were higher (Pα-MHC and miRNA-1 were lower than those in normal group (Pβ-MHC in high-dose group were lower (Pα-MHC and miRNA-1 were higher than those in model group (PConclusion: Leonurine (20 μmol·L-1) could inhibit cardiomyocyte hypertrophy induced by AngⅡ, and the mechanism is related to the inhibition of activation of p38 MAPK signaling pathway and up-regulation the expression of miRNA-1.
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Aim: To investigate the effect of endogenous nociceptin/orphanin FQ(N/OFQ) on arrhythmias induced by myocardial ischemia/reperfusion (I/R) in rats and the role of microRNA-1 (miR-1) in it. Methods: Twenty-four Sprague-Dawley rats were randomly divided into sham-operation group (Sham group), ischemia/reperfusion group (I/R group) and the pretreatment of N/OFQ receptor antagonist (UFP-101) group(U + I/R group). The model of myocardial ischemia/reperfusion was prepared by ligating the left anterior descending branch of the coronary artery of rats. The incidence and arrhythmogenic scores during reperfusion in rats were recorded and analysed. The myocardium at the risk of ischemia was collected at 120 min after reperfusion. MiR-1, GJA1 and KCNJ2 levels were detected by qRT-PCR and Cx43 and kir2. 1 protein levels were detected by Western blot. Results: Antagonism of endogenous N/OFQ could significantly reduce reperfusion arrhythmias and arrhythmogenic scores, compared with I/R group (P < 0. 01). The qRT-PCR and Western blot results suggested that compared with sham group, miR-1 expression significantly increased in I/R group(P < 0. 01), while the expression of Cx43, Cx43 mRNA and kir2. 1 decreased(P< 0. 05); compared with I/R group, pretreatment with UFP-101 led to reduction of miR-1 (P<0. 05) and rise of Cx43 and kir2. 1 (P < 0. 05). Conclusions: Endogenous N/OFQ up-regulates miR-1 and inhibits the expression of Cx43 and kir2. 1 proteins, leading to reperfusion arrhythmias in rats.
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OBJECTIVE To explore the protection mechanism of metformin and tanshinone IIA on myocardial injury. METHODS The cultured neonatal rat ventricular cells (NRVCs) were exposed to 100 μmol·L-1H2O2to simulate the in vitro model of ischemia-reperfusion injury.MTT,TUNEL and Viability/Cytotoxicity Assay were used to evaluate the effect of metformin on the viability of cardiomyocytes after treated with H2O2. The target of miR-1 was verified by Dual luciferase reporter assay. ChIP analyses was adopted to reveal the relationship between C/EBP β and miR-1.Tanshinone IIA was administrated daily for 7 d before ligation of the left anterior descending artery (LAD) and lasted for 3 months after LAD.Whole-cell patch-clamp techniques were used to measure the inward rectifying K+current(IK1)in rat isolated ventricular myocytes.GRP94,p-AMPKα,C/EBP β,CHOP,Caspase-3,Kir2.1,p38 MAPK, Cx43, MEF2 and SRF levels were analyzed by Western blot and miR-1 level was quantified by Real-time PCR.RESULTS The expression of miR-1 was significantly increased in NRVCs exposed to H2O2 in vitro. miR-1 was shown to target the 3′-untranslated region (UTR) of GRP94, which results in the accumulation of un/misfolded proteins,leading to the endoplasmic reticulum(ER)stress.C/EBP β directly induces the upregulation of miR-1 by binding to its promoter.Furthermore,metformin,a direct allosteric AMPK activator, significantly reduces C/EBP β and miR-1 levels comparing with control group. Similarly, tanshinone IIA decreased the incidence of arrhythmias and relieved ischemia-induced injury.Moreover, tanshinone IIA depressed the elevated miR-1 level and inhibited the activation of p38 MAPK and heart special transcription factors SRF and MEF2 in ischemic cardiomyocytes. CONCLUSION Metformin protects cardiomyocytes against H2O2damage through AMPK/C/EBPβ/miR-1/GRP94 pathway.Tanshi-none IIA play a role in protection cardiomyocytes from ischemic injury based on inhibiting miR-1 expres-sion through p38 MAPK signal pathway.
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Objective To evaluate the early diagnostic value of circulating microRNA-1 (miR-1) on acute myocardial infarction (AMI). Methods A prospective cohort study was conducted. The patients with chest pain admitted to the Second People's Hospital of Wuxi from November 2012 to June 2015 were enrolled. According to AMI diagnostic criteria, the patients were divided into AMI group and non-AMI group, and healthy individuals during the same period were served as heath controls. The venous samples of the onset patients were collected within 3 hours after admission. The plasma miR-1 was determined by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR), and the levels of plasma cardiac troponin I (cTnI) and MB isoenzyme of creatine kinase (CK-MB) were measured by electrochemiluminescence. The correlation between plasma miR-1 and cTnI as well as CK-MB was performed by Spearman analysis. The early diagnostic performance of plasma miR-1, cTnI, and CK-MB for AMI was estimated by receiver operating characteristic (ROC) curve analysis. Results There were 127 patients in AMI group, and 107 in non-AMI group, including 82 patients with angina pectoris, 2 with pulmonary embolism, 3 with aortic dissection, 2 with acute pericarditis, 3 with myocarditis, 13 with acute heart failure, and 2 with peptic ulcer. Ninety volunteers were served as healthy controls. There was no difference in clinical characteristics including gender and hyperlipidemia between AMI group and non-AMI group. The expressions of plasma miR-1, cTnI and CK-MB were significantly increased in AMI patients as compared with those of the healthy controls [miR-1 (2-ΔΔCt): 4.32±2.60 vs. 1.44±0.75 and 0.98±0.18, cTnI (μg/L): 3.23 (0.63, 10.70) vs. 0.02 (0.00, 0.17) and 0.00 (0.00, 0.00), CK-MB (U/L): 32.40 (14.20, 95.40) vs. 14.40 (11.20, 17.10) and 8.90 (8.28, 9.50), all P < 0.01]. The expression of plasma miR-1 had a significantly positive correlation with cTnI and CK-MB in AMI patients (r1 = 0.395, r2 = 0.490, both P < 0.000). It was demonstrated by ROC curve analysis that the area under ROC curve (AUC) for the diagnostic value of miR-1 on AMI was 0.905 [95% confidence interval (95%CI) = 0.860-0.950, P = 0.000], the sensitivity was 86.6%, and the specificity was 95.4%; the AUC for cTnI was 0.908 (95%CI = 0.870-0.946, P = 0.000), the sensitivity was 81.9%, and the specificity was 95.9%; the AUC for CK-MB was 0.795 (95%CI = 0.736-0.854, P = 0.000), the sensitivity was 63.0%, and the specificity was 92.9%. Conclusions Plasma miR-1 has the capacity in early diagnosis of AMI, superior to CK-MB, and equal to cTnI. It can provide additional diagnostic information beyond cTnI. The diagnostic accuracy for early AMI can be improved with the combination of plasma miR-1 and cTnI.
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Objective To investigate the changes in plasma microRNA-126 and microRNA-1 in children with asthma exacerbation and its relationship with bronchial asthma.Methods From October 2012 to December 2013,48 children with asthma exacerbation from the Outpatient Department and the Inpatient Department in Houjie Hospital Affiliated to Guangdong Medical College were enrolled in the study (asthma group).Meanwhile,52 healthy children wcre selected as the healthy control group.The expression levels of plasma microRNA-126 and microRNA-1 were detected by real-time quantitative PCR (RT-PCR).The content of interleukin-4 (IL-4) and interferon-γ (IFN-γ) in plasma was measured by enzyme-linked immunosorbent assay (ELISA).The predictive value of microRNA-126 and microRNA-1 in plasma to bronchial asthma was evaluated by receiver operating characteristic (ROC) curve.Results The relative expression levels of plasma microRNA-126 in the asthma group were upregulated compared with those in the healthy control group [7.36 (0.96-41.21) vs 3.68 (0.75-38.91),Z =3.135,P =0.038],and microRNA-1 relative expression levels in the asthma group were lower than those of the healthy control group [2.17 (0.18-26.97) vs 5.83 (0.82-39.62),Z =2.156,P =0.045].The content of IL-4 in asthma group was higher than those of the control group [(109.98 ± 74.58) ng/L vs (78.50 ± 75.82) ng/L,t =2.122,P =0.036],and the IFN-γ level in the asthma group was lower than those of the healthy control group [(70.49 ± 12.03) ng/L vs (77.03 ± 17.16) ng/L,t =2.270,P =0.025].In the plasma of patients with asthma exacerbation,the sensitivity of microRNA-126 and microRNA-1 was 85.42％ (41/48 cases)and 79.17％ (38/48 cases),respectively.The specificity of microRNA-126 and microRNA-1 in healthy controls was 78.85％ (41/52 cases) and 73.08％ (38/52 cases),respectively.The area under ROC curve of microRNA-126 and microRNA-1 was 0.919 (95％ CI 0.866-0.973),0.867 (95％ CI 0.796-0.939).Conclusions MicroRNA-126 is significantly elevated in plasma of children with asthma exacerbation.The plasma levels of microRNA-1 were significantly downregulated.These results suggest that microRNA-126 and microRNA-1 may be potential markers for the diagnosis of bronchial asthma.
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BACKGROUND: Early reperfusion can effectively treat acute myocardial infarction (AMI) and reduce the mortality significantly. This study aimed to compare the role of plasma microRNA-1 (miR-1) and cardiac troponin T (cTnT) in early diagnosis of AMI patients. METHODS: From May 2011 to May 2012, plasma samples were collected from 56 AMI patients and 28 non-AMI controls. The expression of plasma miR-1 was measured by quantitative reverse transcription-polymerase chain reaction (qRT-PCR), and the level of plasma cTnT was measured using electrochemiluminescence-based methods on an Elecsys 2010 Immunoassay Analyzer. SPSS 16.0 was used for the statistical analysis of the results. Data were expressed as mean±standard deviation unless otherwise described. The differences about clinical characteristics between the AMI patients and controls were tested using Student'st test or Fisher's exact test. The Mann-WhitneyU test was conducted to compare the expression of microRNAs between the AMI patients and controls. MicroRNAs expression between different intervals of the AMI patients was compared using Wilcoxon's signed-rank test. The receiver operating characteristic (ROC) curve was established to discriminate the AMI patients from the controls. RESULTS: In the present study, the expression of plasma miR-1 was significantly increased in the AMI patients compared with the healthy controls (P<0.01). The plasma miR-1 in the AMI patients decreased to the normal level at 14 days (P>0.05). The expression of plasma miR-1 was not related to the clinical characteristics of the study population (P>0.05). ROC curve analyses demonstrated that miR-1 was specific and sensitive for the early diagnosis of AMI, but not superior to cTnT. CONCLUSION: Plasma miR-1 could be used in the early diagnosis of AMI, but it is similar to cTnT.
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MicroRNAs (miRs) are endogenous approximately22-nt non-coding RNAs that participate in the regulation of gene expression at post-transcriptional level. MiR-1 is one of the muscle-specific miRs, aberrant expression of miR-1 plays important roles in many physiological and pathological processes. In this review, we focus on the recent studies about miR-1 in cardiac diseases and cancers. The findings indicate that miR-1 may be a novel, important biomarker, and a potential therapeutic target in cardiac diseases and cancers.
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Gene Expression Regulation , Heart Diseases , MicroRNAs , Pathologic Processes , RNA, UntranslatedABSTRACT
Objective To detect the level of plasma microRNA-1 (miR-1) in acute myocardial infarction (AMI) and compare the diagnostic values of it with that of cardiac troponin T (cTnT).Methods During 2011-05 to 2012-05,there were fifty-six plasma samples taken from patients with AMI and twenty-eight plasma specimens got from non-AMI controls were analyzed.The expression of plasma miR-1 was measured by quantitative reverse transcription-polymerase chain reaction (qRT-PCR),and the level of plasma cTnT was measured by using electrochemiluminescence-based methods on the Elecsys 2010 Immunoassay Analyzer.Then,the SPSS 16.0 was used for the statistical analysis.Data were presented as means ± standard deviation unless otherwise described.The differences about clinical characteristics between AMI patients and controls were tested using Student' s t-test or Fisher' s exact test.The Mann-Whitney test was conducted to compare the expression of microRNAs between the AMI patients and controls.The comparison of microRNAs expression between different intervals of AMI patients was done using Wilcoxon signed rank test.The receiver operating characteristic (ROC) curve was established to discriminate AMI patients from controls.Results The expression of plasma miR-1 was significantly increased in AMI patients (P ＜ 0.01) compared with healthy controls.The contents of the plasma miR-1 in AMI patients fell down nearly to the normal level at 14 days (P ＞ 0.05).There was no relevance between the expression of plasma miR-1 and the clinical characteristics of the study population (P ＞ 0.05).Moreover,ROC curve analyses demonstrated that miR-1 had the specificity and sensitivity for the diagnosis of early AMI,but was not superior to cTnT.Conclusions Our results showed that plasma miR-1 had the capacity in early diagnosis of early AMI,and can be biomarker for AMI,however,miR-1 is not superior to cTnT for the diagnosis of AMI.
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Objective To explore the inhibitory effect of calcitonin gene-related peptide (CGRP) on cardiomyocyte apoptosis and the underlying mechanism.Methods In cultured rat cardiomyocytes,apoptosis was induced by the incubation of isoprenaline ( 10ˉ5 mol/L) for 48 h.CGRP ( 10ˉ8 or 10ˉ7 mol/L) was administrated for 1 h before incubating isoprenaline to evaluate its effect on cardiomyocyte apoptosis.At the end of the drug treatment,the rate of apoptotic cells and intracellular reactive oxygen species (ROS) were determined,and RNA was extracted to examine the expression of microRNA-1 and microRNA-133a.Results Isoprenaline significantly increased the rate of apoptotic cells and intracellular ROS production concomitantly with the increased microRNA-1 expression and the decreased microRNA-133a expression,which were inhibited by pretreatment with CGRP.The effects of CGRP were reversed by CGRP receptor antagonist.Conclusion CGRP can inhibit the isoprenaline-induced cardiomyocyte apoptosis.The beneficial effect of CGRP is related to regulating microRNA-1 and microRNA-133a expression through the prevention of isoprenaline-induced ROS production.