ArticleJournal of cellular and molecular medicine2021
Cardiac-specific overexpression of miR-122 induces mitochondria-dependent cardiomyocyte apoptosis and promotes heart failure by inhibiting Hand2.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 39 citations in OpenAlex.
- Noncoding RNA as potential therapeutics to rescue mitochondrial dysfunction in cardiovascular diseases.American journal of physiology. Heart and circulatory physiology · 2025Pooled it
- Crosstalk between microRNA and Oxidative Stress in Heart Failure: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- Bclaf1 drives heart failure by recruiting Srsf2 to enhance Hand2 pre-mRNA splicing and pathological hypertrophy.Nature communications · 2026Article
- Therapeutic potential of ADAR1-regulated macrophage exosomes for improving myocardial damage in septic cardiomyopathy.Journal of nanobiotechnology · 2026Article
- Engineered miR-122 inhibitors preserve endothelial mitochondrial function and prevent vascular dysfunction in obesity-associated prediabetes.Molecular therapy. Nucleic acids · 2026Article
- The MicroRNAs-STAT3-cyclophilin D-cell apoptosis axis: a novel pathway for phosphocreatine treatment in heart disease.Journal of molecular histology · 2026Review
- Exosomes: bridge metabolic regulation in cardiac repair.npj biomedical innovations · 2025Review
- Programmed Cell Death in Heart Failure: Mechanisms, Impacts, and Therapeutic Prospects.Reviews in cardiovascular medicine · 2025Review
- AlkCell communication and signaling : CCS · 2025Article
- Therapeutic Applications of Poly-miRNAs and miRNA Sponges.International journal of molecular sciences · 2025Review
- Advances in MicroRNA Therapy for Heart Failure: Clinical Trials, Preclinical Studies, and Controversies.Cardiovascular drugs and therapy · 2025Review
- Amiodarone Advances the Apoptosis of Cardiomyocytes by Repressing Sigmar1 Expression and Blocking KCNH2-related Potassium Channels.Current molecular medicine · 2025Article
- Bibliometric and visual analysis of miRNAs in heart diseases from 2004 to 2023.Frontiers in cardiovascular medicine · 2025Article
- Circulating myomiRNAs as biomarkers in patients with Cushing's syndrome.Journal of endocrinological investigation · 2024Article
- Small RNA-big impact: exosomal miRNAs in mitochondrial dysfunction in various diseases.RNA biology · 2024Review
- A landscape of mouse mitochondrial small non-coding RNAs.PloS one · 2024Article
- RBM25 regulates hypoxic cardiomyocyte apoptosis through CHOP-associated endoplasmic reticulum stress.Cell stress & chaperones · 2023Article
- miR-122-5p is involved in posttranscriptional regulation of the mitochondrial thiamin pyrophosphate transporter (American journal of physiology. Gastrointestinal and liver physiology · 2023Article
- Review
- The Effects of MicroRNAs in the Development of Heart Failure.Current cardiology reports · 2023Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
MicroRNA-122 (miR-122) is one of several microRNAs elevated in heart failure patients. To investigate the potential role and mechanism of miR-122 in heart failure, we constructed a transgenic mouse overexpressing miR-122 in the heart. This mouse exhibited cardiac dysfunction (as assessed by transthoracic echocardiography), morphological abnormalities of the heart and cardiomyocyte apoptosis characteristic of heart failure. Mechanistically, we identified the Hand2 transcription factor as a direct target of miR-122 using a dual-luciferase reporter assay. In Tg-miR-122 mice and H9C2 cells with miR-122 mimics, we detected apoptosis and increased expression of dynamin-related protein-1 (Drp1). This effect was blocked with prior knockdown of Hand2 in vitro. Our work suggests that miR-122 causes cardiomyocyte apoptosis by inhibiting Hand2 and consequently increasing Drp1-mediated mitochondrial fission. Such a mechanism likely contributes to heart failure and so modulating this pathway could be therapeutically valuable against heart failure.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.