ArticlePLoS biology2018
The microRNA-29/PGC1α regulatory axis is critical for metabolic control of cardiac function.
Article in PLoS biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
49 citing papers in PubMed, 67 citations in OpenAlex.
- Trial
- Beyond the Powerhouse: Mitochondrial Crosstalk as a Master Regulator of Cardiac Metabolic Homeostasis and Failure.Journal of cardiovascular translational research · 2026Review
- Downregulation of microRNA-494 drives mitochondrial biogenesis and function in trained muscle.Experimental physiology · 2026Article
- MicroRNAs in Heart Failure Pathogenesis and Progression: Mechanistic Control, Biomarker Potential, and Translational Perspectives.Life (Basel, Switzerland) · 2026Review
- Psmd13, a proteasome regulatory subunit identified in miR-29a regulation during neuronal differentiation.PloS one · 2026Article
- MiR-199a family members are differentially regulated during physiological and pathological cardiac hypertrophy.Frontiers in physiology · 2026Article
- Orchestrating HFpEF: How Noncoding RNAs Drive Pathophysiology and Phenotypic Outcomes.International journal of molecular sciences · 2025Review
- Role of epicardial adipose tissue in heart failure with preserved ejection fraction: An emerging molecular mechanism and therapeutic potential.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2025Review
- Review
- Aerobic training and vitamin D modulate hepatic miRNA expression to improve lipid metabolism and insulin resistance in type 2 diabetes.Scientific reports · 2025Article
- Restoration of Sestrin 3 Expression Mitigates Cardiac Oxidative Damage in Ischemia-Reperfusion Injury Model.Antioxidants (Basel, Switzerland) · 2025Article
- Circadian system and aging: where both times interact.Frontiers in aging · 2025Review
- Identification and validation of key biomarkers of the glycolysis-ketone body metabolism in heart failure based on multi-omics and machine learning.Frontiers in cardiovascular medicine · 2025Article
- The microRNA-29ab1/Zfp36/AR Axis in the Hypothalamus Regulates Male-Typical Behaviors in Mice.International journal of molecular sciences · 2024Article
- Article
- miR-29 is an important driver of aging-related phenotypes.Communications biology · 2024Article
- MicroRNA-29b Plays a Vital Role in Podocyte Injury and Glomerular Diseases through Inducing Mitochondrial Dysfunction.International journal of biological sciences · 2024Article
- miR-21, miR-221, miR-29 and miR-34 are distinguishable molecular features of a metabolically unhealthy phenotype in young adults.PloS one · 2024Article
- Modulation of miR-29 influences myocardial compliance likely through coordinated regulation of calcium handling and extracellular matrix.Molecular therapy. Nucleic acids · 2023Article
- Article
Corrections and comments
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Authors and funding
20 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Different microRNAs (miRNAs), including miR-29 family, may play a role in the development of heart failure (HF), but the underlying molecular mechanisms in HF pathogenesis remain unclear. We aimed at characterizing mice deficient in miR-29 in order to address the functional relevance of this family of miRNAs in the cardiovascular system and its contribution to heart disease. In this work, we show that mice deficient in miR-29a/b1 develop vascular remodeling and systemic hypertension, as well as HF with preserved ejection fraction (HFpEF) characterized by myocardial fibrosis, diastolic dysfunction, and pulmonary congestion, and die prematurely. We also found evidence that the absence of miR-29 triggers the up-regulation of its target, the master metabolic regulator PGC1α, which in turn generates profound alterations in mitochondrial biogenesis, leading to a pathological accumulation of small mitochondria in mutant animals that contribute to cardiac disease. Notably, we demonstrate that systemic hypertension and HFpEF caused by miR-29 deficiency can be rescued by PGC1α haploinsufficiency, which reduces cardiac mitochondrial accumulation and extends longevity of miR-29-mutant mice. In addition, PGC1α is overexpressed in hearts from patients with HF. Collectively, our findings demonstrate the in vivo role of miR-29 in cardiovascular homeostasis and unveil a novel miR-29/PGC1α regulatory circuitry of functional relevance for cell metabolism under normal and pathological conditions.
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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.