ArticleCell proliferation2025
Elucidating the Role and Mechanism of Alpha-Enolase in Senescent Amelioration via Metabolic Reprogramming.
Article in Cell proliferation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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
6 citing papers in PubMed.
- A Pyrazole-Based Small Molecule, KB3409, Restores Mitochondrial Function via VCP Activation and RCN2-Dependent CaAntioxidants (Basel, Switzerland) · 2026Article
- Ubiquitinated proteomics reveals potential epigenetic-energy metabolism mechanisms in senescent ovarian granulosa cells of advanced maternal age.Journal of assisted reproduction and genetics · 2026Article
- Dysregulation of the glycolysis-mitochondrial metabolism axis in osteoarthritis: mechanisms and therapeutic implications.Journal of orthopaedic translation · 2026Review
- Enolase 1: A paradigm of metabolic enzyme moonlighting in tumorigenesis (Review).International journal of oncology · 2026Review
- Elucidating the Role and Mechanism of Alpha-Enolase in Senescent Amelioration via Metabolic Reprogramming.Cell proliferation · 2025Article
- The methylation site cg06972019 regulates the succinylation-related gene ENO1 to inhibit the occurrence of erectile dysfunction.Hereditas · 2025Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Senescent cells are characterised by increased glycolysis dependence. Normalisation of glycolysis metabolism is essential for senescence amelioration. However, the mechanism of proteins involved in cellular glycolysis metabolism has not been fully elucidated. Here, we identified a candidate compound, an oxazole analogue (KB2764), that can improve senescence. To elucidate the mechanism of the KB2764, we investigated the interacting proteins. KB2764 interacted with alpha-enolase (ENO1) and pyruvate kinase M (PKM), ultimately allowing PKM to phosphorylate ENO1. KB2764 consequently increased mitochondrial ATP production and reduced reliance on glycolysis. Knockdown of the ENO1 experiment in senescent cells demonstrates that regulation of ENO1 activity is a prerequisite for recovery of mitochondrial function. Furthermore, the action of KB2764 extends its application to extend the lifespan of Caenorhabditis elegans. Taken together, our findings reveal a novel mechanism by which senescence is ameliorated through metabolic reprogramming and mitochondrial functional recovery via KB2764-mediated regulation of ENO1 protein activity.
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Registered trials
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