ArticleRedox biology2024
ROS-mediated cytoplasmic localization of CARM1 induces mitochondrial fission through DRP1 methylation.
Article in Redox biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- SIRT3-mediated DRP1 acetylation changes are associated with the restoration of mitochondrial function and alleviation of anterior cruciate ligament injury-induced osteoarthritis.Journal of molecular histology · 2026Article
- Reactive oxygen species in thoracic aortic dissection: Insights into mechanisms and disease progression.Redox biology · 2026Review
- Dynamic regulation of the 'mitochondria‑immune axis' in myocardial infarction: Molecular mechanisms driving macrophage polarization through energy metabolism disorders (Review).Molecular medicine reports · 2026Review
- Protein arginine methyltransferases coordinate mitochondrial stress adaptation and neuromuscular function.Experimental & molecular medicine · 2026Review
- Review
- Review
- KDM4A Erases the H3R17me2a Mark, Facilitating Chromosome Condensation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Protein arginine methyltransferases in cancer: mechanisms, functions, and therapeutic opportunities.Journal of biomedical science · 2026Review
- Mitochondrial quantity-quality imbalance in cellular senescence: practical readouts and minimal assay bundles.BMB reports · 2026Review
- Reversible arginine methylation regulates mitochondrial IDH2 activity: coordinated control by CARM1 and KDM3A/4A.Cell death & disease · 2026Article
- Modeling ovarian cancer chemoresistance: establishment of murine ID8 sublines and elucidation of adaptive mechanisms.Frontiers in oncology · 2026Article
- Functionalized hydrocaffeic acid-chitosan/EGTA hydrogel rescues mitochondrial dysfunction for immunomodulation and joint repair in rheumatoid arthritis.Materials today. Bio · 2025Article
- Ecm19 coordinates mitochondrial fission and cellular redox homeostasis.Redox report : communications in free radical research · 2025Article
- Mechanical confinement induces ferroptosis through mitochondrial dysfunction.Nature communications · 2025Article
- Cardiac dysfunction due to mitochondrial impairment assessed by human iPS cells caused by DNM1L mutations.Pediatric research · 2025Article
- Context-specific applications of CARM1 inhibitors: functional profiles of EZM2302 and TP-064.Molecular medicine (Cambridge, Mass.) · 2025Article
- Reversible arginine methylation of PI3KC2α controls mitotic spindle dynamics.Cell communication and signaling : CCS · 2025Article
- Multifaceted roles of CARM1 beyond histone arginine methylation.Experimental & molecular medicine · 2025Review
- Perspectives on mitochondrial dysfunction in the regeneration of aging skeletal muscle.Cellular & molecular biology letters · 2025Review
- DDX1 methylation mediated MATR3 splicing regulates intervertebral disc degeneration by initiating chromatin reprogramming.Nature communications · 2025Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
The dynamic regulation of mitochondria through fission and fusion is essential for maintaining cellular homeostasis. In this study, we discovered a role of coactivator-associated arginine methyltransferase 1 (CARM1) in mitochondrial dynamics. CARM1 methylates specific residues (R403 and R634) on dynamin-related protein 1 (DRP1). Methylated DRP1 interacts with mitochondrial fission factor (Mff) and forms self-assembly on the outer mitochondrial membrane, thereby triggering fission, reducing oxygen consumption, and increasing reactive oxygen species (ROS) production. This sets in motion a feedback loop that facilitates the translocation of CARM1 from the nucleus to the cytoplasm, enhancing DRP1 methylation and ROS production through mitochondrial fragmentation. Consequently, ROS reinforces the CARM1-DRP1-ROS axis, resulting in cellular senescence. Depletion of CARM1 or DRP1 impedes cellular senescence by reducing ROS accumulation. The uncovering of the above-described mechanism fills a missing piece in the vicious cycle of ROS-induced senescence and contributes to a better understanding of the aging process.
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