ArticlePloS one2013
microRNA-22 promotes heart failure through coordinate suppression of PPAR/ERR-nuclear hormone receptor transcription.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 88 citations in OpenAlex.
- MicroRNAs and Long Non-coding RNAs Associated With Sirtuin Pathways in Myocardial Ischemia/Reperfusion Injury.Cardiovascular drugs and therapy · 2026Review
- Different Pattern in Circulating MicroRNA-22-3p Levels Between Patients With Primary Versus Secondary Sarcopenia.Aging cell · 2025Article
- The crosstalk between MicroRNAs and sirtuins: a bit unexpected therapeutic target for cardiovascular diseases.European journal of medical research · 2025Review
- The Role of microRNA-22 in Metabolism.International journal of molecular sciences · 2025Review
- Effect of miR-1285-3p as a diagnostic biomarker for chronic heart failure on vascular endothelial cells : (Effect of miR-1285-3p as a biomarker for CHF on HUVECs).Journal of cardiothoracic surgery · 2025Article
- MicroRNA: unveiling novel mechanistic and theranostic pathways in diabetic cardiomyopathy.Frontiers in pharmacology · 2025Review
- Human Aging and Age-Related Diseases: From Underlying Mechanisms to Pro-Longevity Interventions.Aging and disease · 2024Review
- Selected miRNA and Psoriasis-Cardiovascular Disease (CVD)-Overweight/Obesity Network-A Pilot Study.International journal of molecular sciences · 2023Article
- Plasma hsa-miR-22-3p Might Serve as an Early Predictor of Ventricular Function Recovery after ST-Elevation Acute Myocardial Infarction.Biomedicines · 2023Article
- Suppression of RBFox2 by Multiple MiRNAs in Pressure Overload-Induced Heart Failure.International journal of molecular sciences · 2023Article
- Review
- SIRT3 protects bovine mammary epithelial cells from heat stress damage by activating the AMPK signaling pathway.Cell death discovery · 2021Article
- MicroRNAs and Calcium Signaling in Heart Disease.International journal of molecular sciences · 2021Review
- Atrial Fibrillation in Heart Failure Is Associated with High Levels of Circulating microRNA-199a-5p and 22-5p and a Defective Regulation of Intracellular Calcium and Cell-to-Cell Communication.International journal of molecular sciences · 2021Article
- Tissue and circulating microRNAs as biomarkers of response to obesity treatment strategies.Journal of endocrinological investigation · 2021Review
- miRNA-22 deletion limits white adipose expansion and activates brown fat to attenuate high-fat diet-induced fat mass accumulation.Metabolism: clinical and experimental · 2021Article
- MiR-29a Increase in Aging May Function as a Compensatory Mechanism Against Cardiac Fibrosis Through SERPINH1 Downregulation.Frontiers in cardiovascular medicine · 2021Article
- microRNAs involved in psoriasis and cardiovascular diseases.Vascular biology (Bristol, England) · 2021Review
- Inhibiting miR-22 Alleviates Cardiac Dysfunction by Regulating Sirt1 in Septic Cardiomyopathy.Frontiers in cell and developmental biology · 2021Article
- Aging, MicroRNAs, and Heart Failure.Current problems in cardiology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
Abstract
Increasing evidence suggests that microRNAs are intimately involved in the pathophysiology of heart failure. MicroRNA-22 (miR-22) is a muscle-enriched miRNA required for optimum cardiac gene transcription and adaptation to hemodynamic stress by pressure overload in mice. Recent evidence also suggests that miR-22 induces hypertrophic growth and it is oftentimes upregulated in end stage heart failure. However the scope of mRNA targets and networks of miR-22 in the heart failure remained unclear. We analyzed transgenic mice with enhanced levels of miR-22 expression in adult cardiomyocytes to identify important pathophysiologic targets of miR-22. Our data shows that forced expression of miR-22 induces a pro-hypertrophic gene expression program, and it elicits contractile dysfunction leading to cardiac dilation and heart failure. Increased expression of miR-22 impairs the Ca(2+) transient, Ca(2+) loading into the sarcoplasmic reticulum plus it interferes with transcription of estrogen related receptor (ERR) and PPAR downstream genes. Mechanistically, miR-22 postranscriptionally inhibits peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α), PPARα and sirtuin 1 (SIRT1) expression via a synergistic circuit, which may account for deleterious actions of unchecked miR-22 expression on the heart.
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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.