ArticlePloS one2014
MicroRNA-208a increases myocardial fibrosis via endoglin in volume overloading heart.
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 31 papers.
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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.
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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, 62 citations in OpenAlex.
- Cardiomyocyte-specific LARP6 overexpression prevents angiotensin II-induced myocardial dysfunction and interstitial fibrosis.American journal of physiology. Heart and circulatory physiology · 2025Article
- Implications of Activating the ANT2/mTOR/PGC-1α Feedback Loop: Insights into Mitochondria-Mediated Injury in Hypoxic Myocardial Cells.Current issues in molecular biology · 2023Article
- MicroRNA expression profiles in familial hypertrophic cardiomyopathy with myosin-binding protein C3 (MYBPC3) gene mutations.BMC cardiovascular disorders · 2022Article
- The miR-214-3p/c-Ski axis modulates endothelial-mesenchymal transition in human coronary artery endothelial cells in vitro and in mice model in vivo.Human cell · 2022Article
- Circulating MicroRNAs and myocardial involvement severity in chronic Chagas cardiomyopathy.Frontiers in cellular and infection microbiology · 2022Article
- Current Knowledge of MicroRNAs (miRNAs) in Acute Coronary Syndrome (ACS): ST-Elevation Myocardial Infarction (STEMI).Life (Basel, Switzerland) · 2021Review
- The Involvement of MicroRNAs in SARS-CoV-2 Infection Comorbid with HIV-Associated Preeclampsia.Current hypertension reports · 2021Review
- Analysis of MicroRNA Profile Alterations in Extracellular Vesicles From Mesenchymal Stromal Cells Overexpressing Stem Cell Factor.Frontiers in cell and developmental biology · 2021Article
- Hyperbaric oxygen-induced long non-coding RNA MALAT1 exosomes suppress MicroRNA-92a expression in a rat model of acute myocardial infarction.Journal of cellular and molecular medicine · 2020Article
- Downregulated PEG3 ameliorates cardiac fibrosis and myocardial injury in mice with ischemia/reperfusion through the NF-κB signaling pathway.Journal of bioenergetics and biomembranes · 2020Article
- microRNA Expression Profiles in Myocardium of High-Fat Diet-Induced Obesity Rat.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Article
- Down-regulation of long non-coding RNA HOTAIR inhibits invasion and migration of oesophageal cancer cells via up-regulation of microRNA-204.Journal of cellular and molecular medicine · 2019Article
- Upregulation of miR-29b-3p protects cardiomyocytes from hypoxia-induced apoptosis by targeting TRAF5.Cellular & molecular biology letters · 2019Article
- Differential Transcriptome Profile and Exercise Capacity in Cardiac Remodeling by Pressure Overload versus Volume Overload.Journal of cardiovascular imaging · 2019Article
- Biomarkers, myocardial fibrosis and co-morbidities in heart failure with preserved ejection fraction: an overview.Archives of medical science : AMS · 2018Article
- MicroRNAs Associated With Reverse Left Ventricular Remodeling in Humans Identify Pathways of Heart Failure Progression.Circulation. Heart failure · 2018Article
- TGF-β Signaling in Control of Cardiovascular Function.Cold Spring Harbor perspectives in biology · 2018Review
- The Role of Endoglin in Myocardial Fibrosis.Acta Cardiologica Sinica · 2017Review
- MicroRNA applications for prostate, ovarian and breast cancer in the era of precision medicine.Endocrine-related cancer · 2017Review
- Altered microRNA expression profiles in lung damage induced by nanosized SiOBioengineered · 2017Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA-208a (mir-208a) is essential for cardiac hypertrophy and fibrosis. Endoglin, a co-receptor of transforming growth factor-β is also essential for cardiac fibrosis. Endoglin has been shown to be a target of mir-208a in the in vitro mechanical stress model. Volume overload can lead to heart failure and cardiac fibrosis. The role of mir-208a and endoglin in volume overload heart failure is well known. We sought to investigate the mechanism of regulation of mir-208a and endoglin in volume overload-induced heart failure. Aorta-caval (AV) shunt was performed in adult Sprague-Dawley rats to induce volume overload. Heart weight and heart weight/body weight ratio significantly increased in AV shunt animals. AV shunt significantly increased left ventricular end-diastolic dimension as compared to sham group. Mir-208a was significantly induced by AV shunt from 3 to 14 days. Endoglin, myosin heavy chain-β and brain natriuretic peptide were significantly induced by AV shunt from 3 to 14 days. Overexpression of mir-208a in the sham group without AV shunt significantly increased endoglin expression similar to the AV shunt group. Antagomir-208a attenuated the endoglin expression induced by AV shunt. Pretreatment with atorvastatin also attenuated the endoglin expression induced by AV shunt. AV shunt significantly increased myocardial fibrosis as compared to sham group. Overexpression of mir-208a in the sham group significantly increased myocardial fibrosis. Antagomir-208a and atorvastatin significantly attenuated the myocardial fibrosis induced by AV shunt. In conclusion, mir-208a increased endoglin expression to induce myocardial fibrosis in volume overloaded heart failure. Treatment with atorvastatin can attenuate the myocardial fibrosis induced by volume overload through inhibition of endoglin expression.
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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.