ArticleJCI insight2023
Myocardial fibrosis and calcification are attenuated by microRNA-129-5p targeting Asporin and Sox9 in cardiac fibroblasts.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
The trial behind it
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Who cites it
29 citing papers in PubMed, 32 citations in OpenAlex.
- The landscape of allele-specific expression in human kidneys.Science advances · 2026Article
- Hepatic stellate cell enriched Asporin drives liver fibrosis by stabilizing ERH to promote IL-17/MAPK11 signaling.Acta pharmaceutica Sinica. B · 2026Article
- Machine learning combined with multi-omics analysis: identifying nucleotide metabolism-associated immune genes and validating their functions in cardiomyopathy.BMC cardiovascular disorders · 2026Article
- Asporin regulates glycolysis and stemness of gastric cancer cells.Journal of molecular histology · 2026Article
- Single cell atlas decodes the molecular dynamics of scar repair after human rotator cuff tear.Bone research · 2026Article
- The silent dialogue between cells: regulatory roles of non-coding RNAs in cardiovascular disease.Frontiers in cell and developmental biology · 2026Review
- Pathogenic glycosyltransferase genes and potential therapeutic drugs in pressure overload-induced heart failure.ESC heart failure · 2025Article
- Multiomic and electrophysiologic analyses reveal that an inherited MRC2 variant causes fibroblast dysfunction and increased atrial fibrillation susceptibility.American journal of physiology. Heart and circulatory physiology · 2025Article
- Recent advances in the design and development of small-molecule MMP-2 inhibitors.Future medicinal chemistry · 2025Review
- Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025Review
- Differential Impacts on Proteoglycan Expression in the Response to Lens Wounding in Reparative and Pro-fibrotic Microenvironments.Proteoglycan research · 2025Article
- Decoding the regulatory roles of circular RNAs in cardiac fibrosis.Non-coding RNA research · 2025Review
- Myocardial ferroptosis may exacerbate the progression of atrial fibrillation through isolevuglandins.European journal of medical research · 2025Review
- SOX9: a key transcriptional regulator in organ fibrosis.Frontiers in pharmacology · 2025Review
- Single-cell RNA-seq uncovers lineage-specific regulatory alterations of fibroblasts and endothelial cells in ligamentum flavum hypertrophy.Frontiers in immunology · 2025Article
- Identification of key genes for heart failure in dilated cardiomyopathy in different populations.Frontiers in genetics · 2025Article
- Single cell deciphering of pruritic keloids: the interaction between fibroblasts and Schwann cells through the Midkine signaling.Burns & trauma · 2025Article
- Epigenetic modifications in cardiac fibrosis: recent evidence of new pharmacological targets.Frontiers in molecular biosciences · 2025Review
- The Complex Role of Matrix Metalloproteinase-2 (MMP-2) in Health and Disease.International journal of molecular sciences · 2024Review
- Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Myocardial fibrosis and calcification associate with adverse outcomes in nonischemic heart failure. Cardiac fibroblasts (CF) transition into myofibroblasts (MF) and osteogenic fibroblasts (OF) to promote myocardial fibrosis and calcification. However, common upstream mechanisms regulating both CF-to-MF transition and CF-to-OF transition remain unknown. microRNAs are promising targets to modulate CF plasticity. Our bioinformatics revealed downregulation of miR-129-5p and upregulation of its targets small leucine-rich proteoglycan Asporin (ASPN) and transcription factor SOX9 as common in mouse and human heart failure (HF). We experimentally confirmed decreased miR-129-5p and enhanced SOX9 and ASPN expression in CF in human hearts with myocardial fibrosis and calcification. miR-129-5p repressed both CF-to-MF and CF-to-OF transition in primary CF, as did knockdown of SOX9 and ASPN. Sox9 and Aspn are direct targets of miR-129-5p that inhibit downstream β-catenin expression. Chronic Angiotensin II infusion downregulated miR-129-5p in CF in WT and TCF21-lineage CF reporter mice, and it was restored by miR-129-5p mimic. Importantly, miR-129-5p mimic not only attenuated progression of myocardial fibrosis, calcification marker expression, and SOX9 and ASPN expression in CF but also restored diastolic and systolic function. Together, we demonstrate miR-129-5p/ASPN and miR-129-5p/SOX9 as potentially novel dysregulated axes in CF-to-MF and CF-to-OF transition in myocardial fibrosis and calcification and the therapeutic relevance of miR-129-5p.
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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.