ArticleJournal of molecular and cellular cardiology2020
Nuclear-mitochondrial communication involving miR-181c plays an important role in cardiac dysfunction during obesity.
Article in Journal of molecular and cellular cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Sex differences in mitochondrial CaJournal of molecular and cellular cardiology · 2026Article
- HuR-driven reversible mitochondrial shuttling buffers cytosolic miRNA levels in hepatic cells.The Journal of biological chemistry · 2026Article
- Male obesity causes adipose mitochondrial dysfunction in FNature communications · 2026Article
- The Role of MicroRNAs in Mitochondrial Homeostasis and their Involvement in the Pathogenesis of Obesity and Metabolic Syndrome: A Focus on MicroRNAs.Current medicinal chemistry · 2026Review
- Mechanisms of microRNA trafficking to mitochondria in the heart.Current opinion in physiology · 2025Article
- Review
- Mitochondrial microRNAs (mitomiRs) as emerging biomarkers and therapeutic targets for chronic human diseases.Frontiers in genetics · 2025Review
- Sex-dependent phosphorylation of Argonaute 2 reduces the mitochondrial translocation of miR-181c and induces cardioprotection in females.Journal of molecular and cellular cardiology · 2024Article
- Review
- Role of Specificity Protein 1 (SP1) in Cardiovascular Diseases: Pathological Mechanisms and Therapeutic Potentials.Biomolecules · 2024Review
- MICU3 Regulates Mitochondrial Calcium and Cardiac Hypertrophy.Circulation research · 2024Article
- MicroRNA-181 in cardiovascular disease: Emerging biomarkers and therapeutic targets.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Review
- Role of post-translational modifications of Sp1 in cardiovascular diseases.Frontiers in cell and developmental biology · 2024Review
- Divergent cardiac and renal effects of miR-181c-5p inhibition in a rodent heart failure model.Frontiers in cardiovascular medicine · 2024Article
- The miR-181 family: Wide-ranging pathophysiological effects on cell fate and function.Journal of cellular physiology · 2023Review
- Mitochondrial quality control in health and cardiovascular diseases.Frontiers in cell and developmental biology · 2023Review
- MicroRNAs in cardiovascular diseases.Medical review (2021) · 2022Review
- Mitochondrial calcium exchange in physiology and disease.Physiological reviews · 2022Review
- Research progress on the relationship between mitochondrial function and heart failure: A bibliometric study from 2002 to 2021.Frontiers in molecular biosciences · 2022Article
- Difluoromethylornithine attenuates isoproterenol-induced cardiac hypertrophy by regulating apoptosis, autophagy and the mitochondria-associated membranes pathway.Experimental and therapeutic medicine · 2021Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
aimsIn cardiomyocytes, there is microRNA (miR) in the mitochondria that originates from the nuclear genome and matures in the cytoplasm before translocating into the mitochondria. Overexpression of one such miR, miR-181c, can lead to heart failure by stimulating reactive oxygen species (ROS) production and increasing mitochondrial calcium level ([Ca METHODS AND
resultsWe used an in vivo mouse model of high-fat diet (HFD) for 18 weeks and induced high lipid load in H9c2 cells with oleate-conjugated bovine serum albumin in vitro. We tested the cardioprotective role of lowering miR-181c by using miR-181c/d
conclusionThis study has identified a unique nuclear-mitochondrial communication mechanism in the heart orchestrated by miR-181c. Obesity-induced overexpression of miR-181c increases [Ca
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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.