ArticlePloS one2014
Regulation of cardiac expression of the diabetic marker microRNA miR-29.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 2 of them syntheses that pooled it.
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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
51 citing papers in PubMed, 2 syntheses or guidelines pooled it, 74 citations in OpenAlex.
- The expression profiles and roles of microRNAs in cardiac glucose metabolism.Frontiers in endocrinology · 2025Pooled it
- Pooled it
- Predicting and understanding the response to short-term intensive insulin therapy in people with early type 2 diabetes.Molecular metabolism · 2019Trial
- Cardiovascular Dysfunction in Type 2 Diabetes: The Role of MicroRNAs.Handbook of experimental pharmacology · 2026Review
- MicroRNA: unveiling novel mechanistic and theranostic pathways in diabetic cardiomyopathy.Frontiers in pharmacology · 2025Review
- Exploring the Causal Link Between Autoimmune Diseases and Pulmonary Arterial Hypertension: A Bidirectional Mendelian Randomization Study.Global heart · 2025Article
- MicroRNAs Targeting Critical Molecular Pathways in Diabetic Cardiomyopathy Emerging Valuable for Therapy.Cardiovascular & hematological agents in medicinal chemistry · 2024Review
- Article
- Article
- Glucagon-Like Peptide-1 Receptor Agonist Protects Against Diabetic Cardiomyopathy by Modulating microRNA-29b-3p/SLMAP.Drug design, development and therapy · 2023Article
- Effects of non-coding RNAs and RNA-binding proteins on mitochondrial dysfunction in diabetic cardiomyopathy.Frontiers in cardiovascular medicine · 2023Review
- Exosomal microRNAs miR-30d-5p and miR-126a-5p Are Associated with Heart Failure with Preserved Ejection Fraction in STZ-Induced Type 1 Diabetic Rats.International journal of molecular sciences · 2022Article
- The role of miR-29 family in disease.Journal of cellular biochemistry · 2021Review
- Molecular Mechanisms and Epigenetic Regulation in Diabetic Cardiomyopathy.Frontiers in cardiovascular medicine · 2021Review
- miR-208a in Cardiac Hypertrophy and Remodeling.Frontiers in cardiovascular medicine · 2021Review
- Pregnancy-associated cardiac dysfunction and the regulatory role of microRNAs.Biology of sex differences · 2020Review
- Assessment of Cell-Free Long Non-Coding RNA-H19 and miRNA-29a, miRNA-29b Expression and Severity of Diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Article
- Non-coding RNA involvement in the pathogenesis of diabetic cardiomyopathy.Journal of cellular and molecular medicine · 2019Review
- A therapeutic approach towards microRNA29 family in vascular diabetic complications: A boon or curse?Journal of diabetes and metabolic disorders · 2019Article
- HIF-1 regulation of miR-29c impairs SERCA2 expression and cardiac contractility.American journal of physiology. Heart and circulatory physiology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Diabetes mellitus (DM) is an independent risk factor for heart disease and its underlying mechanisms are unclear. Increased expression of diabetic marker miR-29 family miRNAs (miR-29a, b and c) that suppress the pro-survival protein Myeloid Cell Leukemia 1(MCL-1) is reported in pancreatic β-cells in Type 1 DM. Whether an up-regulation of miR-29 family miRNAs and suppression of MCL-1 (dysregulation of miR-29-MCL-1 axis) occurs in diabetic heart is not known. This study tested the hypothesis that insulin regulates cardiac miR-29-MCL-1 axis and its dysregulation correlates with DM progression. In vitro studies with mouse cardiomyocyte HL-1 cells showed that insulin suppressed the expression of miR-29a, b and c and increased MCL-1 mRNA. Conversely, Rapamycin (Rap), a drug implicated in the new onset DM, increased the expression of miR-29a, b and c and suppressed MCL-1 and this effect was reversed by transfection with miR-29 inhibitors. Rap inhibited mammalian target of rapamycin complex 1 (mTORC1) signaling in HL-1 cells. Moreover, inhibition of either mTORC1 substrate S6K1 by PF-4708671, or eIF4E-induced translation by 4E1RCat suppressed MCL-1. We used Zucker diabetic fatty (ZDF) rat, a rodent model for DM, to test whether dysregulation of cardiac miR-29-MCL-1 axis correlates with DM progression. 11-week old ZDF rats exhibited significantly increased body weight, plasma glucose, insulin, cholesterol, triglycerides, body fat, heart weight, and decreased lean muscle mass compared to age-matched lean rats. Rap treatment (1.2 mg/kg/day, from 9-weeks to 15-weeks) significantly reduced plasma insulin, body weight and heart weight, and severely dysregulated cardiac miR-29-MCL1 axis in ZDF rats. Importantly, dysregulation of cardiac miR-29-MCL-1 axis in ZDF rat heart correlated with cardiac structural damage (disorganization or loss of myofibril bundles). We conclude that insulin and mTORC1 regulate cardiac miR-29-MCL-1 axis and its dysregulation caused by reduced insulin and mTORC1 inhibition increases the vulnerability of a diabetic heart to structural damage.
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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.