Evidence map›Paper›PMID 41236095›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Targeting Endothelial KDM5A to Attenuate Aging and Ameliorate Age-Associated Metabolic Abnormalities.

Rifeng Gao, Lifeng Liang, Ling Yang, Chunyu Lyu, Yang Lyu, Weijun Yang, Jiaran Shi, Wei Wei, Jiahui Cheng, Xiaolei Sun and 12 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

22 authors.

Rifeng GaoDepartment of Cardiac Surgery, The Second Affiliated Hospital, Zhejiang University, Hangzhou, 310009, China.
Lifeng LiangDepartment of Cardiology, Cardiovascular Center, Beijing Friendship Hospital, Capital Medical University, Beijing, 100029, China.
Ling YangDepartment of Ultasonography, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Chunyu LyuSchool of Nursing, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Yang LyuDepartment of Cardiology, Shanghai Fifth People's Hospital, Fudan University, Shanghai, 200240, China.
Weijun YangDepartment of Cardiac Surgery, The Second Affiliated Hospital, Zhejiang University, Hangzhou, 310009, China.
Jiaran ShiDepartment of Cardiology, Lihuili Hospital Facilitated to Ningbo University, Ningbo, 315048, China.
Wei WeiDepartment of Ultasonography, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Jiahui ChengDepartment of Radiology, Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Xiaolei SunDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, 200232, China.
Xian ZhuDepartment of Cardiac Surgery, The Second Affiliated Hospital, Zhejiang University, Hangzhou, 310009, China.
Chao ChenDepartment of Cardiac Surgery, The Second Affiliated Hospital, Zhejiang University, Hangzhou, 310009, China.
Xiaoting XuDepartment of Cardiac Surgery, The Second Affiliated Hospital, Zhejiang University, Hangzhou, 310009, China.
Jianchuang QiDepartment of Cardiac Surgery, The Second Affiliated Hospital, Zhejiang University, Hangzhou, 310009, China.
Wenli LiDepartment of Radiology, Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Yizhe ZhangDepartment of Anesthesiology, Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Xiao ZhangDepartment of Anesthesiology, Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Yan ZhouDepartment of Radiology, Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Aiqiang DongDepartment of Cardiac Surgery, The Second Affiliated Hospital, Zhejiang University, Hangzhou, 310009, China.
Juntao ChenDepartment of Urology, The Second Affiliated Hospital, Zhejiang University, Hangzhou, 310009, China.
Bo LiDepartment of Radiology, Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.ORCID https://orcid.org/0000-0001-9476-3073
Kun YangDepartment of Cardiac Surgery, The Second Affiliated Hospital, Zhejiang University, Hangzhou, 310009, China.

Funding

2025 Zhejiang Natural Science Foundation LQN25H250002General Funding of China Postdoctoral Science Foundation 2024M752875Key research and development program of Zhejiang Province 2025C02143National Natural Science Foundation of China 82170332National Natural Science Foundation of China 82400884Natural Science Foundation of Shanghai Municipality 24ZR1448200Renji Hospital Crosswise Project RJKY23-003Shanghai Science and Technology Committee Project 24ZR1444600
6 · The paper itself

Abstract

Vascular aging accelerates the gradual deterioration of systemic organ function, yet its key driving factors are still largely unexplored. Here, it is demonstrated that lysine-specific demethylase 5A (KDM5A) decreases and histone H3 lysine 4 (H3K4me3) increases in vascular endothelial cells (VECs) isolated from ageing mice and VEC senescence models. KDM5A deficiency exacerbated endothelial cell aging in vitro. Endothelial-specific KDM5A-deficient mice exhibit shortened lifespan and multiple senescent phenotypes, including fat accumulation, reduced thermogenic capacity, skeletal kyphosis, and age-related liver lesions, while maintaining VECs-specific KDM5A levels attenuates these adverse metabolic abnormalities and prolongs lifespan. Mechanistically, endothelial KDM5A deficiency aggravates aging-associated fatty acid (FA) metabolism disorders by enhancing H3K4me3 enrichment at the promoter region of FA-binding protein 4 (FABP4), which leads to active FABP4 transcription. Together, the study reveals the regulatory mechanisms of KDM5A in age-dependent metabolic disorders and identifies KDM5A/FABP4 axis as a potential therapeutic target for vascular aging and related organ dysfunction.

Indexed as

AgingEndothelial CellsMetabolic DiseasesRetinoblastoma-Binding Protein 2AnimalsCellular SenescenceFatty Acid-Binding ProteinsHistonesHumansMaleMiceMice, Inbred C57BLMice, KnockoutFabp4 protein, mouseFatty Acid-Binding ProteinsHistonesRetinoblastoma-Binding Protein 2agingFABP4KDM5Ametabolic abnormalitiesvascular endothelial cells

Identifiers

PMID41236095
PMCPMC12866742

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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 OpenQuestion graph.