ArticleOxidative medicine and cellular longevity2019
miR-154-5p Functions as an Important Regulator of Angiotensin II-Mediated Heart Remodeling.
Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 27 citations in OpenAlex.
- Global research trends of cell death in diabetic cardiomyopathy from 2000 to 2024: a bibliometric analysis and integrative overview.Journal of cardiothoracic surgery · 2026Review
- Transcriptomic Profiling of MicroRNA and Non-Coding RNA from Whole Blood of African Americans with MASLD.International journal of molecular sciences · 2026Article
- Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025Review
- Efficacy of Semaglutide in Modulating Cardiac Remodeling in Mice: A Review of Mechanisms and Outcomes.Research in heart yield and translational medicine · 2025Review
- Screening and Evaluation of tRF-Glu-CTC-013 as a Biomarker and Key Regulator in the Development of Cardiac Hypertrophy.International journal of medical sciences · 2025Article
- DEAD-box helicase 17 (DDX17) protects cardiac function by promoting mitochondrial homeostasis in heart failure.Signal transduction and targeted therapy · 2024Article
- Therapeutic Potential of EVs: Targeting Cardiovascular Diseases.Biomedicines · 2023Review
- Profound Impact of Decline in N-Acetylgalactosamine-4-Sulfatase (Arylsulfatase B) on Molecular Pathophysiology and Human Diseases.International journal of molecular sciences · 2022Review
- Molecular environment and atypical function: What do we know about enzymes associated with Mucopolysaccharidoses?Orphanet journal of rare diseases · 2022Review
- Circulating exo-miR-154-5p regulates vascular dementia through endothelial progenitor cell-mediated angiogenesis.Frontiers in cellular neuroscience · 2022Article
- miR-488-3p Protects Cardiomyocytes against Doxorubicin-Induced Cardiotoxicity by Inhibiting CyclinG1.Oxidative medicine and cellular longevity · 2022Article
- MicroRNA-128b mediates lipopolysaccharide-induced apoptosis via reactive oxygen species in human pulmonary microvascular endothelial cells.Clinics (Sao Paulo, Brazil) · 2022Article
- Anti-Arrhythmic Effects of Sodium-Glucose Co-Transporter 2 Inhibitors.Frontiers in pharmacology · 2022Review
- A comparative analysis of heart microRNAs in vertebrates brings novel insights into the evolution of genetic regulatory networks.BMC genomics · 2021Article
- Targeting the microRNA-34a as a Novel Therapeutic Strategy for Cardiovascular Diseases.Frontiers in cardiovascular medicine · 2021Review
- Ferulic Acid Alleviates Oxidative Stress-Induced Cardiomyocyte Injury by the Regulation of miR-499-5p/Evidence-based complementary and alternative medicine : eCAM · 2021Article
- An Insight on Multicentric Signaling of Angiotensin II in Cardiovascular system: A Recent Update.Frontiers in pharmacology · 2021Review
- MiR-154-5p-MCP1 Axis Regulates Allergic Inflammation by Mediating Cellular Interactions.Frontiers in immunology · 2021Article
- Cardiac Aging: From Basic Research to Therapeutics.Oxidative medicine and cellular longevity · 2021Review
- MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases.International journal of molecular sciences · 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 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic hypertension, valvular heart disease, and heart infarction cause cardiac remodeling and potentially lead to a series of pathological and structural changes in the left ventricular myocardium and a progressive decrease in heart function. Angiotensin II (AngII) plays a key role in the onset and development of cardiac remodeling. Many microRNAs (miRNAs), including miR-154-5p, may be involved in the development of cardiac remolding, but the underlying molecular mechanisms remain unclear. We aimed to characterize the function of miR-154-5p and reveal its mechanisms in cardiac remodeling induced by AngII. First, angiotensin II led to concurrent increases in miR-154-5p expression and cardiac remodeling in adult C57BL/6J mice. Second, overexpression of miR-154-5p to a level similar to that induced by AngII was sufficient to trigger cardiomyocyte hypertrophy and apoptosis, which is associated with profound activation of oxidative stress and inflammation. Treatment with a miR-154-5p inhibitor noticeably reversed these changes. Third, miR-154-5p directly inhibited arylsulfatase B (Arsb) expression by interacting with its 3'-UTR and promoted cardiomyocyte hypertrophy and apoptosis. Lastly, the angiotensin type 1 receptor blocker telmisartan attenuated AngII-induced cardiac hypertrophy, apoptosis, and fibrosis by blocking the increase in miR-154-5p expression. Moreover, upon miR-154-5p overexpression in isolated cardiomyocytes, the protective effect of telmisartan was partially abolished. Based on these results, increased cardiac miR-154-5p expression is both necessary and sufficient for AngII-induced cardiomyocyte hypertrophy and apoptosis, suggesting that the upregulation of miR-154-5p may be a crucial pathological factor and a potential therapeutic target for cardiac remodeling.
Indexed as
Identifiers
What OpenQuestion holds
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.