Evidence mapPaperPMID 39609696Full record

ArticleJournal of translational medicine2024

Inhibition of the E3 ligase UBR5 stabilizes TERT and protects vascular organoids from oxidative stress.

Haijing Zhao, Nian Cao, Qi Liu, Yingyue Zhang, Rui Jin, Huiying Lai, Li Zheng, Honghong Zhang, Yue Zhu, Yuhan Ma and 6 more

Abstract read
In one paragraph

Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Multicellular senescence programs in the aged heart.Journal of molecular and cellular cardiology plus · 2026
    Review
  3. Review
  4. Article
  5. 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

16 authors.

Haijing Zhao *Department of Cardiology, the Sixth Medical Centre, Chinese PLA General Hospital, Beijing, 100037, People's Republic of China.
Nian Cao *Department of Cardiology, the Sixth Medical Centre, Chinese PLA General Hospital, Beijing, 100037, People's Republic of China.
Qi Liu *Medical School of Chinese PLA, Chinese PLA General Hospital, Beijing, 100853, People's Republic of China.
Yingyue ZhangDepartment of Cardiology, the Sixth Medical Centre, Chinese PLA General Hospital, Beijing, 100037, People's Republic of China.
Rui JinBeijing Institute of Biotechnology, Beijing, 100850, People's Republic of China.
Huiying LaiDepartment of Clinical Laboratory, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, 100730, People's Republic of China.
Li ZhengSchool of Medicine, Nankai University, Tianjin, 300071, People's Republic of China.
Honghong ZhangDepartment of Cardiology, the Sixth Medical Centre, Chinese PLA General Hospital, Beijing, 100037, People's Republic of China.
Yue ZhuDepartment of Cardiology, the Sixth Medical Centre, Chinese PLA General Hospital, Beijing, 100037, People's Republic of China.
Yuhan MaSchool of Medicine, Nankai University, Tianjin, 300071, People's Republic of China.
Zengao YangSchool of Medicine, South China University of Technology, Guangzhou, 510006, People's Republic of China.
Zhengfeng WuDepartment of Cardiology, the Sixth Medical Centre, Chinese PLA General Hospital, Beijing, 100037, People's Republic of China.
Weini LiDepartment of Biomedical Science, Cedars-Sinai Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, USA.
Yuqi LiuDepartment of Cardiology, the Sixth Medical Centre, Chinese PLA General Hospital, Beijing, 100037, People's Republic of China. ametuofo980869@163.com.ORCID 0000-0001-5792-5723
Long ChengThe Key Laboratory of Geriatrics, Institute of Geriatric Medicine, Beijing Institute of Geriatrics, Chinese Academy of Medical Sciences, Beijing Hospital/National Centre of Gerontology of National Health Commission, Beijing, 100730, People's Republic of China. biolongcheng@outlook.com.
Yundai ChenDepartment of Cardiology, the Sixth Medical Centre, Chinese PLA General Hospital, Beijing, 100037, People's Republic of China. cyundai@vip.163.com.

Funding

Basic Strengthening Plan Project 2023-JCJQ-JJ-0704Beijing Nova Program Z191100001119020China Postdoctoral Science Foundation 2022M723897China Postdoctoral Science Foundation 2023T160787National High Level Hospital Clinical Research Funding 2023-1National High Level Hospital Clinical Research Funding BJ-2024-219National Key Research and Development Program of China 2022YFC3600100National Natural Science Foundation of China 82070434/H0214National Natural Science Foundation of China 82072717National Natural Science Foundation Regional Innovation and Development Joint Fund U23A6011
6 · The paper itself

Abstract

backgroundExcessive oxidative stress is known to cause endothelial dysfunction and drive cardiovascular diseases (CVD). While telomerase reverse transcriptase (TERT) shows protective effects against oxidative stress in rodents and is associated to human flow-mediated dilation in CVD, its regulatory mechanisms in human vascular systems under pathological oxidative stress require further investigation.

methodsHuman induced pluripotent stem cells (hiPSCs) were used to create vascular organoids (VOs). These VOs and human umbilical vein endothelial cells (HUVECs) were subjected to oxidative stress through both hydrogen peroxide (H

resultsROS significantly impaired VO development and endothelial progenitor cell (EPC) angiogenesis, evidenced by reduced neovascular sprouting and increased senescence markers, including elevated SA-β-Gal activity and SASP-related cytokine levels. Overexpression of TERT counteracted these effects, restoring VO development and EPC function. Immunoprecipitation-mass spectrometry identified UBR5 as a critical TERT regulator, facilitating its degradation. Inhibition of UBR5 stabilized TERT, improving VO angiogenic capacity, and reducing SA-β-Gal activity and SASP cytokine levels.

conclusionsInhibiting UBR5 stabilizes TERT, which preserves EPC angiogenic capacity, reduces VO impairment, and delays endothelial cell senescence under oxidative stress. These findings highlight the potential of targeting UBR5 to enhance vascular health in oxidative stress-related conditions.

Indexed as

Cellular SenescenceHuman Umbilical Vein Endothelial CellsInduced Pluripotent Stem CellsOrganoidsOxidative StressTelomeraseUbiquitin-Protein LigasesBlood VesselsHumansHydrogen PeroxideNeovascularization, PhysiologicProtein StabilityReactive Oxygen SpeciesHydrogen PeroxideReactive Oxygen SpeciesTelomeraseTERT protein, humanUbiquitin-Protein LigasesUBR5 protein, humanOxidative stressSenescenceTERTUBR5Vascular organoids

Identifiers

PMID39609696
PMCPMC11605888

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.