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Role of long noncoding RNAs in pathological cardiac remodeling after myocardial infarction: An emerging insight into molecular mechanisms and therapeutic potential.
Yaghoobi, Alireza; Rezaee, Malihe; Behnoush, Amir Hossein; Khalaji, Amirmohammad; Mafi, Alireza; Houjaghan, Amirmasoud Kazemzadeh; Masoudkabir, Farzad; Pahlavan, Sara.
Affiliation
  • Yaghoobi A; Tehran Heart Center, Cardiovascular Diseases Research Institute, Tehran University of Medical Sciences, Tehran, Iran; Department of Pharmacology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
  • Rezaee M; Tehran Heart Center, Cardiovascular Diseases Research Institute, Tehran University of Medical Sciences, Tehran, Iran; Department of Pharmacology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
  • Behnoush AH; Tehran Heart Center, Cardiovascular Diseases Research Institute, Tehran University of Medical Sciences, Tehran, Iran.
  • Khalaji A; Tehran Heart Center, Cardiovascular Diseases Research Institute, Tehran University of Medical Sciences, Tehran, Iran.
  • Mafi A; Department of Clinical Biochemistry, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran.
  • Houjaghan AK; School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
  • Masoudkabir F; Tehran Heart Center, Cardiovascular Diseases Research Institute, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: tehran.centerheart@yahoo.com.
  • Pahlavan S; Department of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran. Electronic address: sarapahlavan@royaninstitute.org.
Biomed Pharmacother ; 172: 116248, 2024 Mar.
Article in En | MEDLINE | ID: mdl-38325262
ABSTRACT
Myocardial infarction (MI) is the leading cause of heart failure (HF), accounting for high mortality and morbidity worldwide. As a consequence of ischemia/reperfusion injury during MI, multiple cellular processes such as oxidative stress-induced damage, cardiomyocyte death, and inflammatory responses occur. In the next stage, the proliferation and activation of cardiac fibroblasts results in myocardial fibrosis and HF progression. Therefore, developing a novel therapeutic strategy is urgently warranted to restrict the progression of pathological cardiac remodeling. Recently, targeting long non-coding RNAs (lncRNAs) provided a novel insight into treating several disorders. In this regard, numerous investigations have indicated that several lncRNAs could participate in the pathogenesis of MI-induced cardiac remodeling, suggesting their potential therapeutic applications. In this review, we summarized lncRNAs displayed in the pathophysiology of cardiac remodeling after MI, emphasizing molecular mechanisms. Also, we highlighted the possible translational role of lncRNAs as therapeutic targets for this condition and discussed the potential role of exosomes in delivering the lncRNAs involved in post-MI cardiac remodeling.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: RNA, Long Noncoding / Heart Failure / Myocardial Infarction Limits: Humans Language: En Journal: Biomed Pharmacother Year: 2024 Document type: Article Affiliation country:

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: RNA, Long Noncoding / Heart Failure / Myocardial Infarction Limits: Humans Language: En Journal: Biomed Pharmacother Year: 2024 Document type: Article Affiliation country: