ArticleNature metabolism2026
PFKM governs metabolic shifts throughout skeletal muscle differentiation.
Article in Nature metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Article
- PFKM Modulates Porcine Skeletal Muscle Satellite Cell Differentiation Through Metabolic and Mitochondrial Pathways.Veterinary sciences · 2026Article
- Article
- Inhibition of Ornithine Decarboxylase 1 Mitigates Denervation-Induced Muscle Atrophy by Suppressing Proteolysis and Preserving Muscle Stem Cell Homeostasis.Cell proliferation · 2026Article
Corrections and comments
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Authors and funding
23 authors.
Funding
Abstract
Metabolism is known to influence cell identity, but the underlying mechanisms remain unclear. Here we reveal spatiotemporal dynamics of phosphofructokinase 1 (PFK1), a key glycolytic enzyme, within the skeletal muscle lineage. The expression of PFKM (the muscle isoform of PFK1) is low in muscle stem cells and increases during differentiation. Mechanistically, Wnt signalling rapidly induces lysosomal degradation of PFKM through a methyl arginine degron motif, which gets selectively methylated by the protein arginine methyltransferase (PRMT1) and delivered to lysosomes through microautophagy. PFKM degradation shifts glucose metabolism from glycolysis to the pentose phosphate pathway. PFKM overexpression increases glycolysis and promotes differentiation into terminally differentiated myofibres. On the other hand, PFKM knockdown blunts differentiation, which can be rescued by supplementation with the downstream glycolytic intermediate 3-phosphoglycerate. In sum, our findings highlight the importance of compartmentalized metabolism in cell fate decisions.
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Registered trials
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