Evidence map›Paper›PMID 33082910›Full record

ArticleOxidative medicine and cellular longevity2020

Interaction of TPPP3 with VDAC1 Promotes Endothelial Injury through Activation of Reactive Oxygen Species.

Naijia Liu, Yintao Li, Wu Nan, Wenbai Zhou, Jinya Huang, Rumei Li, Linuo Zhou, Renming Hu

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 28% of its field
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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Biochemistry and biophysics reports · 2026
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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

8 authors at 4 institutions in 2 countries.

Naijia LiuDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.
Yintao LiDepartment of Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, China.
Wu NanDepartment of Geriatrics, Zhongshan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Wenbai ZhouDepartment of Medicine, Emanuel Medical Center, Turlock, California, USA.
Jinya HuangDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.
Rumei LiDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.
Linuo ZhouDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0002-8558-1347
Renming HuDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0002-7742-2602
Fudan University · CNLegacy Emanuel Medical Center · USShandong Tumor Hospital · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial injury plays a critical role in the pathogenesis of cardiovascular disorders and metabolic-associated vascular complications which are the leading cause of death worldwide. However, the mechanism underlying endothelial dysfunction is not completely understood. The study is aimed at investigating the role of tubulin polymerization-promoting protein family member 3 (TPPP3) in palmitic acid- (PA-) induced endothelial injury. The effect of TPPP3 on human umbilical vein endothelial cells (HUVECs) was determined by evaluating apoptosis, tube formation, and reactive oxygen species (ROS) production. TPPP3 silencing inhibited PA overload-induced apoptosis and production of ROS, along with the alteration of apoptosis-related key proteins such as BCL-2 and Bax. Mechanically, voltage-dependent anion channel 1 (VDAC1) was identified as a novel functional binding partner of TPPP3, and TPPP3 promoted VDAC1 protein stability and its activity. Further studies indicated that TPPP3 could promote apoptosis, ROS production, tube formation, and proapoptotic protein expression and reduce antiapoptotic protein expression through increasing VDAC1 expression under mildly elevated levels of PA. Collectively, these results demonstrated that TPPP3 could promote PA-induced oxidative damage in HUVECs via a VDAC1-dependent pathway, suggesting that TPPP3 might be considered as a potential therapeutic target in vascular disease.

Indexed as

Apoptosisbcl-2-Associated X ProteinCytoskeletal ProteinsHumansHuman Umbilical Vein Endothelial CellsNeovascularization, PhysiologicOxidative StressPalmitic AcidProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesRNA InterferenceRNA, Small InterferingUp-RegulationVoltage-Dependent Anion Channel 1bcl-2-Associated X ProteinBCL2 protein, humanCytoskeletal ProteinsPalmitic AcidProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesRNA, Small InterferingTPPP3 protein, humanVDAC1 protein, humanVoltage-Dependent Anion Channel 1

Identifiers

PMID33082910
PMCPMC7556057
OpenAlexW3089744246

What OpenQuestion 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 OpenQuestion graph.