{"title":"研究miRNA-137-3p/383-5p/PGC-1α信号通路对心肌肥厚的治疗潜力。","authors":"Khadam Hussain, Somia Khurram, Muhammad Yousaf, Ayesha Ishtiaq, Iram Mushtaq, Tahir Ali, Iram Murtaza","doi":"10.1007/s12265-025-10636-9","DOIUrl":null,"url":null,"abstract":"<p><p>Pathological growth of cardiomyocytes known as cardiac hypertrophy (CH). Differential expressions of miRNAs have an immense therapeutic potential against cardiac hypertrophy. The current study aim is to evaluate the therapeutic potential of miRNA-137-3p/383-5p in cardiac hypertrophy by regulation of PGC-1α signaling nexus. Silencing of pro-hypertrophic miRNAs e.g. miR-137-3p and miR-383-5p leads to the restoration of their common target gene PGC-1α in hypertrophic cells. Interestingly, the results of this invivo study showed the cardioprotective effects of these antagomirs. Moreover, PGC-1α associated signaling events e.g. fatty acid oxidation (Cpt1a, Cpt1b), mitochondria membrane potential (MMP), mitochondrial reactive oxygen species (mtROS), oxidative phosphorylation (Ndufa6, Atp5me), apoptosis (Bcl-2, BAX), antioxidants (SOD, GSH, CAT), mitochondrial dynamic (Mfn-2, Drp-1) were significantly restored in the treated groups of miRNA antagomirs. Conclusively, this study uncovers that the pharmacological inhibition of miR-137-3p and miR-383-5p have a potential to rescue from the cardiac hypertrophy by regulation of PGC-1α signaling nexus.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":""},"PeriodicalIF":2.4000,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Investigating the Therapeutic Potential of miRNA-137-3p/383-5p/PGC-1α Signalling Nexus Against Cardiac Hypertrophy.\",\"authors\":\"Khadam Hussain, Somia Khurram, Muhammad Yousaf, Ayesha Ishtiaq, Iram Mushtaq, Tahir Ali, Iram Murtaza\",\"doi\":\"10.1007/s12265-025-10636-9\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Pathological growth of cardiomyocytes known as cardiac hypertrophy (CH). Differential expressions of miRNAs have an immense therapeutic potential against cardiac hypertrophy. The current study aim is to evaluate the therapeutic potential of miRNA-137-3p/383-5p in cardiac hypertrophy by regulation of PGC-1α signaling nexus. Silencing of pro-hypertrophic miRNAs e.g. miR-137-3p and miR-383-5p leads to the restoration of their common target gene PGC-1α in hypertrophic cells. Interestingly, the results of this invivo study showed the cardioprotective effects of these antagomirs. Moreover, PGC-1α associated signaling events e.g. fatty acid oxidation (Cpt1a, Cpt1b), mitochondria membrane potential (MMP), mitochondrial reactive oxygen species (mtROS), oxidative phosphorylation (Ndufa6, Atp5me), apoptosis (Bcl-2, BAX), antioxidants (SOD, GSH, CAT), mitochondrial dynamic (Mfn-2, Drp-1) were significantly restored in the treated groups of miRNA antagomirs. Conclusively, this study uncovers that the pharmacological inhibition of miR-137-3p and miR-383-5p have a potential to rescue from the cardiac hypertrophy by regulation of PGC-1α signaling nexus.</p>\",\"PeriodicalId\":15224,\"journal\":{\"name\":\"Journal of Cardiovascular Translational Research\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":2.4000,\"publicationDate\":\"2025-06-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Cardiovascular Translational Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s12265-025-10636-9\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"CARDIAC & CARDIOVASCULAR SYSTEMS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Cardiovascular Translational Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s12265-025-10636-9","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
Investigating the Therapeutic Potential of miRNA-137-3p/383-5p/PGC-1α Signalling Nexus Against Cardiac Hypertrophy.
Pathological growth of cardiomyocytes known as cardiac hypertrophy (CH). Differential expressions of miRNAs have an immense therapeutic potential against cardiac hypertrophy. The current study aim is to evaluate the therapeutic potential of miRNA-137-3p/383-5p in cardiac hypertrophy by regulation of PGC-1α signaling nexus. Silencing of pro-hypertrophic miRNAs e.g. miR-137-3p and miR-383-5p leads to the restoration of their common target gene PGC-1α in hypertrophic cells. Interestingly, the results of this invivo study showed the cardioprotective effects of these antagomirs. Moreover, PGC-1α associated signaling events e.g. fatty acid oxidation (Cpt1a, Cpt1b), mitochondria membrane potential (MMP), mitochondrial reactive oxygen species (mtROS), oxidative phosphorylation (Ndufa6, Atp5me), apoptosis (Bcl-2, BAX), antioxidants (SOD, GSH, CAT), mitochondrial dynamic (Mfn-2, Drp-1) were significantly restored in the treated groups of miRNA antagomirs. Conclusively, this study uncovers that the pharmacological inhibition of miR-137-3p and miR-383-5p have a potential to rescue from the cardiac hypertrophy by regulation of PGC-1α signaling nexus.
期刊介绍:
Journal of Cardiovascular Translational Research (JCTR) is a premier journal in cardiovascular translational research.
JCTR is the journal of choice for authors seeking the broadest audience for emerging technologies, therapies and diagnostics, pre-clinical research, and first-in-man clinical trials.
JCTR''s intent is to provide a forum for critical evaluation of the novel cardiovascular science, to showcase important and clinically relevant aspects of the new research, as well as to discuss the impediments that may need to be overcome during the translation to patient care.