ArticleMolecular therapy : the journal of the American Society of Gene Therapy2022
CircRNA Samd4 induces cardiac repair after myocardial infarction by blocking mitochondria-derived ROS output.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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Who cites it
82 citing papers in PubMed, 139 citations in OpenAlex.
- Human induced pluripotent stem cell-derived cardiomyocyte patch enhances cardiac regeneration in a J2N-k hamster model of dilated cardiomyopathy.Regenerative therapy · 2026Article
- The emerging roles of small nucleolar RNAs, piwi-interacting RNAs, tRNA-derived small RNAs, and circular RNAs in the regulation of cardiac hypertrophy, ischemic heart disease, and heart failure.Genes & diseases · 2026Review
- Downregulation of circ_0001112 Enhances Myocardial Infarction Through Regulation of miR-324-5p/CDK6 Axis.Journal of biochemical and molecular toxicology · 2026Article
- Circular RNAs in Cardiovascular Diseases: From Regulatory Networks to Functional Effectors.International journal of molecular sciences · 2026Review
- Multi-Omics and Artificial Intelligence in Cardiovascular Medicine: From Mechanistic Insights to Clinical Translation.Biomedicines · 2026Review
- CircRNA-regulated programmed cell death networks in cardiomyocytes: Molecular crosstalk and therapeutic translation.Non-coding RNA research · 2026Review
- Circular RNA-mediated regulation of key signaling pathways in cardiovascular diseases: a review.Journal of advanced research · 2026Review
- Hsa_circ_0007158 promotes colorectal cancer progression via the ceRNA axis and its association with immune infiltration.Cancer cell international · 2026Article
- Remodeling of the circRNA Landscape in Myocardial Infarction Integrates Nuclear Regulation, DNA Damage Response, and Cardiomyocyte Structural Pathways.Biomolecules · 2026Article
- CircLOC375190 Promotes Mitochondrial Dysfunction and Ferroptosis in Neurons after Stroke by Stabilizing HUWE1 Through Interaction-Induced Ubiquitination and Degradation of IGF2BP2.Applied biochemistry and biotechnology · 2026Article
- Long non-coding RNAs as modulators of metabolic reprogramming for endogenous heart regeneration: Mechanisms and therapeutic potential.Biomedical journal · 2026Review
- CircATXN2 exacerbates pulmonary arterial hypertension by modulating the miR-138-5p/SMURF1 axis.Respiratory research · 2026Article
- CircPDXDC1 Induces Mitochondrial Dysfunction and Autophagy Dysfunction in Acute Myocardial Infarction by Promoting ELAVL1 Ubiquitination.Applied biochemistry and biotechnology · 2026Article
- ROS-Mediated Cardiomyocyte Proliferation and Myocardial Regeneration: Mechanisms and Targeted Strategies for Ischemic Heart Disease.Journal of cardiovascular development and disease · 2026Review
- The silent dialogue between cells: regulatory roles of non-coding RNAs in cardiovascular disease.Frontiers in cell and developmental biology · 2026Review
- The many faces of p97/Cdc48 in mitochondrial homeostasis.Essays in biochemistry · 2025Review
- Histone acetyltransferase 1 promotes postinfarction inflammatory response by regulation of monocyte histone succinylation.Nature communications · 2025Article
- Circular RNA circDhx32 promotes cardiac inflammatory responses in mouse cardiac ischemia-reperfusion injury via binding to FOXO1 competed with AdipoR1.Acta pharmacologica Sinica · 2025Article
- A review: oxidative stress in skeletal muscle and the non-coding RNAs behind it.Molecular and cellular biochemistry · 2025Review
- Dysregulated Redox Signaling and Its Impact on Inflammatory Pathways, Mitochondrial Dysfunction, Autophagy and Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2025Review
22 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) derived from oxygen-dependent mitochondrial metabolism are the essential drivers of cardiomyocyte (CM) cell-cycle arrest in adulthood. Mitochondria-localized circular RNAs (circRNAs) play important roles in regulating mitochondria-derived ROS production, but their functions in cardiac regeneration are still unknown. Herein, we investigated the functions and underlying mechanism of mitochondria-localized circSamd4 in cardiac regeneration. We found that circSamd4 was selectively expressed in fetal and neonatal CMs. The transcription factor Nrf2 controlled circSamd4 expression by binding to the promoter of circSamd4 host gene. CircSamd4 overexpression reduced while circSamd4 silenced increased mitochondrial oxidative stress and subsequent oxidative DNA damage. Moreover, circSamd4 overexpression induced CM proliferation and prevented CM apoptosis, which reduced the size of the fibrotic area and improved cardiac function after myocardial infarction (MI). Mechanistically, circSamd4 reduced oxidative stress generation and maintained mitochondrial dynamics by inducing the mitochondrial translocation of the Vcp protein, which downregulated Vdac1 expression and prevented the mitochondrial permeability transition pore (mPTP) from opening. Our findings suggest that circSamd4 is a novel therapeutic target for heart failure after MI.
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