ArticleAutophagy2025
PRMT1 (protein arginine methyltransferase 1) is essential for neuromuscular junction and mitochondrial homeostasis via mitophagy regulation.
Article in Autophagy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed.
- Phase-transition failure in aged skeletal muscle regeneration.Biogerontology · 2026Review
- Protein arginine methyltransferases coordinate mitochondrial stress adaptation and neuromuscular function.Experimental & molecular medicine · 2026Review
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The neuromuscular junction (NMJ) is essential for transmitting neural stimulus to muscles, triggering muscle contraction. Mitochondria are enriched in NMJ to support the energy needs required for neuromuscular function and stability. Thus, maintaining mitochondrial homeostasis through the clearance of damaged mitochondria, a process known as mitophagy, is vital for preserving neuromuscular health. Here, we highlight the crucial role of muscle PRMT1 in maintaining NMJ and mitochondrial homeostasis via mitophagy regulation. PRMT1 is distinctively expressed in myofibers, accumulating in the postsynaptic area, with its levels upregulated in denervated muscles. PRMT1-ablated muscles displayed disrupted NMJs and an accumulation of abnormal mitochondria, accompanied by increased mitochondrial oxidative stress. Additionally,
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