Evidence map›Paper›PMID 41037021›Full record

ArticleAging cell2025

TRPM7 Deficiency Accelerates Vascular Senescence by Inhibiting H3K18 Lactylation.

Yue Wang, Jing Chen, Xuan Wang, Jin Li, Shujun Yang, Lingping Zhu, Zhenyu Li, Chuanchang Li, Wanzhou Wu, Yongping Bai

Abstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Yue WangDepartment of Geriatric Medicine, Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Jing ChenNational Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Xuan WangDepartment of Geriatric Medicine, Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Jin LiDepartment of Cardiology, Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Shujun YangNational Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Lingping ZhuDepartment of Geriatric Medicine, Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Zhenyu LiDepartment of Geriatric Medicine, Xiangya Hospital, Central South University, Changsha, People's Republic of China.ORCID 0000-0002-9285-0277
Chuanchang LiDepartment of Geriatric Medicine, Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Wanzhou WuDepartment of Geriatric Medicine, Xiangya Hospital, Central South University, Changsha, People's Republic of China.ORCID 0000-0002-4017-6399
Yongping BaiDepartment of Geriatric Medicine, Xiangya Hospital, Central South University, Changsha, People's Republic of China.ORCID 0000-0002-6355-5842

Funding

Hunan Provincial Major Basic Research Program 2025JC0001Hunan Provincial Natural Science Foundation of China 2025JJ60510Key Research and Development Program of Hunan Province of China 2023SK2018Major Project of Natural Science Foundation of Hunan Province 2021JC0002National Key Research and Development Program of China 2022YFC2010004National Natural Science Foundation of China 82171579National Natural Science Foundation of China 82270446National Natural Science Foundation of China 82325006National Natural Science Foundation of China 82371577Noncommunicable Chronic Diseases-National Science and Technology Major Project 2023ZD0503202
6 · The paper itself

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.

Indexed as

Cellular SenescenceHistonesProtein Serine-Threonine KinasesTRPM Cation ChannelsAnimalsEndothelial CellsHumansMiceMice, Inbred C57BLMice, KnockoutHistonesProtein Serine-Threonine KinasesTrpm7 protein, mouseTRPM Cation ChannelsH3K18histone lactylationTRPM7vascular aging

Identifiers

PMID41037021
PMCPMC12611325

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.