ArticleAging cell2025
TRPM7 Deficiency Accelerates Vascular Senescence by Inhibiting H3K18 Lactylation.
Article in Aging cell, 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Review
- The metabolic-epigenetic landscape of aging: interplay between histone acetylation, lactylation, and glycation.Frontiers in aging · 2026Review
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Authors and funding
10 authors.
Funding
Abstract
Blood vessels exhibit a pronounced vulnerability to aging and are often at the forefront of systemic aging processes. Vascular endothelial cells, which line blood vessels and directly contact blood flow, are susceptible to damage and play a key role in vascular aging; however, the underlying mechanisms of their aging remain unclear. Here, we identify TRPM7 as a key molecule in vascular endothelial aging. Endothelial deletion of TRPM7 significantly accelerates premature vascular aging in mice. Mechanistically, TRPM7 deficiency reduces lactate production and inhibits the lactylation writer protein p300, leading to decreased histone H3K18 lactylation. This induces a gene expression profile reprogramming, increasing the expression of the senescence gene p21 and decreasing the expression of angiogenesis genes. Inhibiting p21 or supplementing lactate reversed premature vascular endothelial aging caused by TRPM7 deficiency. This study reveals the critical role of the TRPM7-H3K18la axis in vascular aging, offering potential therapeutic targets for vascular anti-aging interventions.
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