ArticleCardiovascular research2022
MicroRNA-27b-3p down-regulates FGF1 and aggravates pathological cardiac remodelling.
Article in Cardiovascular research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Noncoding RNA as potential therapeutics to rescue mitochondrial dysfunction in cardiovascular diseases.American journal of physiology. Heart and circulatory physiology · 2025Pooled it
- Review
- Xanthatin Attenuates Angiotensin II-Induced Cardiac Hypertrophy by Targeting CREB5.Journal of cardiovascular translational research · 2026Article
- Circulating miR-16 as an Early Biomarker of Subclinical Myocardial Strain Impairment in Pediatric Primary Hypertension.International journal of molecular sciences · 2026Article
- MicroRNAs in Heart Failure Pathogenesis and Progression: Mechanistic Control, Biomarker Potential, and Translational Perspectives.Life (Basel, Switzerland) · 2026Review
- Article
- [Advances on efficacy and mechanisms of acid fibroblast growth factor for promoting injured tissue repair].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2026Review
- Biochanin A Mitigates Pressure Overload-Induced Cardiac Hypertrophy Through Modulation of the NF-κB/Cbl-b/NLRP3 Signaling Axis.Cardiovascular drugs and therapy · 2026Article
- Platycodin D alleviates cardiac hypertrophy in the treatment of heart failure by inhibiting p53-dependent BCL-2/Bax/caspase-3 signaling pathway.Frontiers in pharmacology · 2026Article
- Cardiomyocyte-derived OTUD7B promotes cardiac hypertrophy by deubiquitinating SERCA2a.Theranostics · 2026Article
- Nanoparticle-Based Therapeutic Strategies for Pathological Cardiac Hypertrophy: Preclinical Advances, Translational Challenges, and Future Perspectives.International journal of nanomedicine · 2026Review
- circSP199a, a circularized RNA sponge targeting miR-199a-5p and -3p, mitigates mouse cardiac hypertrophy and fibrosis.Acta pharmacologica Sinica · 2026Article
- FGF9 alleviates diabetic cardiomyopathy by activating Nrf2 via SQSTM1/p62-Keap1 in mice.Communications biology · 2025Article
- Preliminary identification of the MiR-548ah-5p/THBD axis for heart failure via DirectTarget causal framework and bioinformatics analysis.European journal of medical research · 2025Article
- The role of CARMA3 in regulating fibrosis to prevent hypertrophic cardiomyopathy.Cell death discovery · 2025Article
- Anticoagulation Therapies and microRNAs in Heart Failure.Biomolecules · 2025Review
- The significance of small noncoding RNAs in the pathogenesis of cardiovascular diseases.Genes & diseases · 2025Review
- Microrna363-5p targets thrombospondin3 to regulate pathological cardiac remodeling.Molecular and cellular biochemistry · 2025Article
- Myocardial ferroptosis may exacerbate the progression of atrial fibrillation through isolevuglandins.European journal of medical research · 2025Review
- MiR-133b-3p attenuates angiotensin II-induced cardiac hypertrophy through the inhibition of apoptosis by targetingActa biochimica et biophysica Sinica · 2025Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsThe heart undergoes pathological remodelling under increased stress and neuronal imbalance. MicroRNAs (miRNAs) are involved in post-transcriptional regulation of genes in cardiac physiology and pathology. However, the mechanisms underlying miRNA-mediated regulation of pathological cardiac remodelling remain to be studied. This study aimed to explore the function of endogenous microRNA-27b-3p (miR-27b-3p) in pathological cardiac remodelling. METHODS AND
resultsmiR-27b-3p expression was elevated in the heart of a transverse aortic constriction (TAC)-induced cardiac hypertrophy mouse model. miR-27b-knockout mice showed significantly attenuated cardiac hypertrophy, fibrosis, and inflammation induced by two independent pathological cardiac hypertrophy models, TAC and Angiotensin II (Ang II) perfusion. Transcriptome sequencing analysis revealed that miR-27b deletion significantly down-regulated TAC-induced cardiac hypertrophy, fibrosis, and inflammatory genes. We identified fibroblast growth factor 1 (FGF1) as a miR-27b-3p target gene in the heart which was up-regulated in miR-27b-null mice. We found that both recombinant FGF1 (rFGF1) and inhibition of miR-27b-3p enhanced mitochondrial oxidative phosphorylation (OXPHOS) and inhibited cardiomyocyte hypertrophy. Importantly, rFGF1 administration inhibited cardiac hypertrophy and fibrosis in TAC- or Ang II-induced models and enhanced OXPHOS by activating PGC1α/β.
conclusionsOur study demonstrated that miR-27b-3p induces pathological cardiac remodelling and suggests that inhibition of endogenous miR-27b-3p or administration of FGF1 might have the potential to suppress cardiac remodelling in a clinical setting.
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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.