Related Experiment Video
Updated: Jan 13, 2026
09:16
Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
Published on: June 3, 2018
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Cardiometabolic Therapies Shape Non-Coding RNA Landscapes in Cardiovascular Fibrosis
Erica Floris1, Francesco Nutile1, Claudia Cozzolino1
1Department of Medical and Surgical Sciences and Biotechnologies, Sapienza University of Rome, 04100 Latina, Italy.
Metabolites
|October 28, 2025
Summary
Metabolic drugs can reduce heart fibrosis by altering non-coding RNA (ncRNA) expression. This epigenetic regulation offers new therapeutic targets for cardiovascular diseases linked to metabolic syndrome.
Area of Science:
- Cardiovascular Biology
- Epigenetics
- Pharmacology
Background:
- Cardiometabolic syndromes drive cardiovascular fibrosis and heart failure.
- Non-coding RNAs (ncRNAs) like miRNAs, lncRNAs, and circRNAs are key epigenetic regulators of fibrosis.
- Metabolic therapies may influence ncRNA expression, impacting cardiovascular fibrosis.
Purpose of the Study:
- To review the interplay between metabolic therapies and ncRNA regulation in cardiovascular fibrosis.
- To highlight the therapeutic and biomarker potential of microRNAs (miRNAs) in this context.
Main Methods:
- Manual curation and literature search on PubMed for studies on metabolic modulators and ncRNAs.
- Focus on metformin, SGLT2 inhibitors, PPARγ agonists, GLP-1 receptor agonists, and fatty acid oxidation inhibitors.
- Extraction and categorization of data from in vitro, in vivo, and clinical studies.
Main Results:
- Metabolic modulators downregulate pro-fibrotic ncRNAs (e.g., miR-21, H19) and upregulate anti-fibrotic ncRNAs (e.g., miR-29, miR-133a).
- These changes attenuate transforming growth factor-beta (TGF-β) signaling, reducing extracellular matrix accumulation and improving myocardial compliance.
- ncRNA profile changes correlated with improved fibrosis-related endpoints across drug classes.
Conclusions:
- Metabolic modulators exert anti-fibrotic effects via ncRNA regulation.
- This offers novel therapeutic strategies and potential biomarkers for cardiovascular fibrosis in cardiometabolic disease.
- Targeting metabolic-ncRNA crosstalk may lead to precise interventions for pathological cardiac remodeling.
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