ArticleClinical rheumatology2026
High glucose-induced mitophagy accelerates premature aging of T cells in patients with rheumatoid arthritis.
Article in Clinical rheumatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- SIRT7-Mediated H2BK120 Succinylation Drives Aberrant Mitophagy in Sepsis-Associated Cognitive Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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Authors and funding
4 authors.
Funding
Abstract
objectivesPremature T cell aging, marked by telomere shortening and cell cycle arrest, plays a key role in the pathogenesis of rheumatoid arthritis (RA). Growing evidence suggests that high glucose-induced metabolic dysfunction critically regulates both cellular aging and RA progression. This study explores how high glucose exacerbates T cell aging, providing novel insights into the mechanisms underlying RA development.
methodsCD4
resultsRA-derived CD4
conclusionElevated mitophagy induced by high glucose represents a cell-autonomous mechanism driving premature T cell aging in RA, presenting a novel therapeutic avenue for disease management. Key Points • Dysregulated glucose metabolism is a key driver of T cell aging and RA pathogenesis. • High glucose exposure triggers metabolic reprogramming, leading to succinate accumulation. • Accumulated succinate induces ZNF76 succinylation and enhances DRP1-dependent mitophagy-a phenotype consistently observed in CD4+ T cells from RA patients. • DRP1-dependent mitophagy drives T cell aging in RA.
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Registered trials
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