ArticleSignal transduction and targeted therapy2021
The double face of miR-320: cardiomyocytes-derived miR-320 deteriorated while fibroblasts-derived miR-320 protected against heart failure induced by transverse aortic constriction.
Article in Signal transduction and targeted therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- YY1/Asprosin/PFKP axis regulates glycolytic metabolic and exacerbates pathological cardiac hypertrophy.Nature communications · 2026Article
- Circulating Extracellular Vesicles in the Pathogenesis of Heart Failure in Patients With Chronic Kidney Disease.Circulation · 2026Article
- A Molecular Perspective on the Intricate Interplay Among Exosomes, Bioenergetic Metabolism, and the Pathogenesis of Diabetic Cardiomyopathy.Journal of cardiovascular translational research · 2025Review
- Lung-Derived Small Extracellular Vesicles Containing miR-15a-5p/miR-96-5p Promote Myocardial Fibrosis in Hypertrophic Cardiomyopathy via Targeting SMAD7.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- Osteopontin promoted cardiac inflammation through increased interleukin-12 in acute myocarditis.Molecular biomedicine · 2025Article
- Profibrotic Molecules Are Reduced in CRISPR-Edited Emery-Dreifuss Muscular Dystrophy Fibroblasts.Cells · 2025Article
- A neonatal rat model of progressive left ventricular pressure overload induced by abdominal aortic banding microsurgery.JTCVS techniques · 2025Article
- Hepatic stellate cell-specific miR-214 expression alleviates liver fibrosis without boosting steatosis and inflammation.Journal of translational medicine · 2025Article
- Advances in MicroRNA Therapy for Heart Failure: Clinical Trials, Preclinical Studies, and Controversies.Cardiovascular drugs and therapy · 2025Review
- Protosappanin A protects against pathological cardiac hypertrophy by inhibiting oxidative stress and NLRP3 inflammasome-mediated pyroptosis via activation of the Nrf2 signaling pathway.Frontiers in cardiovascular medicine · 2025Article
- MicroRNA and Heart Failure: A Novel Promising Diagnostic and Therapeutic Tool.Journal of clinical medicine · 2024Review
- Plekhm2 acts as an autophagy modulator in murine heart and cardiofibroblasts.Scientific reports · 2024Article
- Nuclear AGO2 promotes myocardial remodeling by activating ANKRD1 transcription in failing hearts.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- The dual effects of miR-222 in cardiac hypertrophy: bridging pathological and physiological paradigms.Cardiovascular research · 2024Article
- Comparative Analysis of Non-Coding RNA Transcriptomics in Heart Failure.Biomedicines · 2022Review
- Inhibition of PLA2G4E/cPLA2 promotes survival of random skin flaps by alleviating Lysosomal membrane permeabilization-Induced necroptosis.Autophagy · 2022Article
- Profiling of Non-Coding Regulators and Their Targets in Epicardial Fat from Patients with Coronary Artery Disease.International journal of molecular sciences · 2022Article
- The dual role of glioma exosomal microRNAs: glioma eliminates tumor suppressor miR-1298-5p via exosomes to promote immunosuppressive effects of MDSCs.Cell death & disease · 2022Article
- Signaling cascades in the failing heart and emerging therapeutic strategies.Signal transduction and targeted therapy · 2022Review
- A Non-Canonical Link between Non-Coding RNAs and Cardiovascular Diseases.Biomedicines · 2022Review
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) are aberrantly expressed in the pathophysiologic process of heart failure (HF). However, the functions of a certain miRNA in different cardiac cell types during HF are scarcely reported, which might be covered by the globe effects of it on the heart. In the current study, Langendorff system was applied to isolate cardiomyocytes (CMs) and cardiac fibroblasts (CFs) from transverse aortic constriction (TAC)-induced mice. Slight increase of miR-320 expression was observed in the whole heart tissue of TAC mice. Interestingly, miR-320 was significantly elevated in CMs but decreased in CFs from TAC mice at different time points. Then, recombinant adeno-associated virus 9 with cell-type-specific promoters were used to manipulate miR-320 expressions in vivo. Both in vitro and in vivo experiments showed the miR-320 overexpression in CMs exacerbated cardiac dysfunction, whereas overexpression of miR-320 in CFs alleviated cardiac fibrosis and hypertrophy. Mechanically, downstream signaling pathway analyses revealed that miR-320 might induce various effects via targeting PLEKHM3 and IFITM1 in CMs and CFs, respectively. Moreover, miR-320 mediated effects could be abolished by PLEKHM3 re-expression in CMs or IFITM1 re-expression in CFs. Interestingly, miR-320 treated CFs were able to indirectly affect CMs function, but not vice versa. Meanwhile, upstream signaling pathway analyses showed that miR-320 expression and decay rate were rigorously manipulated by Ago2, which was regulated by a cluster of cell-type-specific TFs distinctively expressed in CMs and CFs, respectively. Together, we demonstrated that miR-320 functioned differently in various cell types of the heart during the progression of HF.
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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.