ArticleMolecular therapy : the journal of the American Society of Gene Therapy2025
Enhanced fatty acid oxidation via SCD1 downregulation fuels cardiac reprogramming.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Signaling pathways regulating cardiac regeneration.Cell regeneration (London, England) · 2026Review
- Exploring Active Ingredients and Mechanisms ofMolecules (Basel, Switzerland) · 2026Article
- Timing matters: association of persistent postoperative anemia with adverse outcomes in cardiac surgery.Journal of cardiothoracic surgery · 2026Article
- Ptch2 Deficiency Triggers Lipoma Formation and Adipogenic Transcriptome Reprogramming in Nile tilapia (Animals : an open access journal from MDPI · 2026Article
- Metabolic reprogramming in cardiac fibrosis: mechanisms, crosstalk, and therapeutic interventions.Frontiers in physiology · 2026Review
- Blocking nuclear receptor Nr4a3 unlocks the senescence barrier to promote direct cardiac reprogramming.Science advances · 2025Article
- Beclin1 deficiency unlocks cardiac lineage commitment through convergent Wnt and BMP signaling activation.Stem cell research & therapy · 2025Article
- Advances in fibroblast-based cardiac reprogramming in the treatment of heart disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Decoding cardiac metabolic reprogramming through single-cell multi-omics: from mechanisms to therapeutic applications.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Direct cardiac reprogramming has emerged as a promising therapeutic strategy to remuscularize injured myocardium. This approach converts non-contractile fibroblasts to induced cardiomyocytes (iCMs) that spontaneously contract, yet the intrinsic metabolic requirements driving cardiac reprogramming are not fully understood. Using single-cell metabolic flux estimation and flux balance analysis, we characterized the metabolic heterogeneity of iCMs and identified fatty acid oxidation (FAO) as a critical factor in iCM conversion. Both pharmacological and genetic inhibition of FAO impairs iCM generation. We further identified stearoyl-coenzyme A desaturase 1 (SCD1) as a metabolic switch that suppresses iCM reprogramming. Mechanistically, Scd1 knockdown activates PGC1α and PPARβ signaling, enhancing FAO-related gene expression and mitochondrial biogenesis, thereby improving reprogramming efficacy. Pharmacological manipulations targeting SCD1, PGC1α, and the PPARβ signaling axis further improved iCM generation and mitochondrial function. Our findings collectively highlight FAO as a key determinant of iCM fate and offer new therapeutic avenues for advancing reprogramming strategies.
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Registered trials
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