Evidence map›Paper›PMID 38491252›Full record

ArticleApoptosis : an international journal on programmed cell death2024

A self-amplifying loop of TP53INP1 and P53 drives oxidative stress-induced apoptosis of bone marrow mesenchymal stem cells.

Fanchao Li, Fei Zhang, Tao Wang, Zhihong Xie, Hong Luo, Wentao Dong, Jian Zhang, Chao Ren, Wuxun Peng

Open access · hybridAbstract read
In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

17 citing papers in PubMed, 13 citations in OpenAlex.

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  3. In Situ Programmable Modulation of Hydrogel Stiffness for Stage-Adaptive Bone Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 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

9 authors at 2 institutions in 1 country.

Fanchao Li *Department of Orthopedics and Traumatology, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, Guizhou, China.
Fei Zhang *Department of Orthopedics and Traumatology, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, Guizhou, China.
Tao WangDepartment of Orthopedics and Traumatology, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, Guizhou, China.
Zhihong XieDepartment of Orthopedics and Traumatology, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, Guizhou, China.
Hong LuoDepartment of Orthopedics and Traumatology, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, Guizhou, China.
Wentao DongDepartment of Orthopedics and Traumatology, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, Guizhou, China.
Jian ZhangDepartment of Orthopedics and Traumatology, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, Guizhou, China.
Chao RenDepartment of Orthopedics and Traumatology, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, Guizhou, China.
Wuxun PengDepartment of Orthopedics and Traumatology, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, Guizhou, China. 903463644@qq.com.
Guiyang Medical University · CNAffiliated Hospital of Guizhou Medical University · CN

Funding

he Discipline Outstanding Reserve Talent Program of Affiliated Hospital of Guizhou Medical University gyfyxkrc-2023-07the Guizhou Provincial Natural Science Foundation Qiankehebasis-ZK [2022] general 399, Qiankehebasis-ZK [2022] general 447the National Natural Science Foundation of China 82260434, 82060397the NSFC Cultivation Project of Guizhou Medical University 21NSFCP08the Science and Technology Foundation of Guizhou Provincial Health Committee gzwjkj2020-1-130, gzwkj2021-234the Start-up Fund for Doctoral Research at the Affiliated Hospital of Guizhou Medical University gyfybsky-2022-14
6 · The paper itself

Abstract

Bone marrow mesenchymal stem cell (BMSC) transplantation is a promising regenerative therapy; however, the survival rate of BMSCs after transplantation is low. Oxidative stress is one of the main reasons for the high apoptosis rate of BMSCs after transplantation, so there is an urgent need to explore the mechanism of oxidative stress-induced apoptosis of BMSCs. Our previous transcriptome sequencing results suggested that the expression of P53-induced nuclear protein 1 (TP53INP1) and the tumor suppressor P53 (P53) was significantly upregulated during the process of oxidative stress-induced apoptosis of BMSCs. The present study further revealed the role and mechanism of TP53INP1 and P53 in oxidative stress-induced apoptosis in BMSCs. Overexpression of TP53INP1 induced apoptosis of BMSCs, knockdown of TP53INP1 alleviated oxidative stress apoptosis of BMSCs. Under oxidative stress conditions, P53 is regulated by TP53INP1, while P53 can positively regulate the expression of TP53INP1, so the two form a positive feedback loop. To clarify the mechanism of feedback loop formation. We found that TP53INP1 inhibited the ubiquitination and degradation of P53 by increasing the phosphorylation level of P53, leading to the accumulation of P53 protein. P53 can act on the promoter of the TP53INP1 gene and increase the expression of TP53INP1 through transcriptional activation. This is the first report on a positive feedback loop formed by TP53INP1 and P53 under oxidative stress. The present study clarified the formation mechanism of the positive feedback loop. The TP53INP1-P53 positive feedback loop may serve as a potential target for inhibiting oxidative stress-induced apoptosis in BMSCs.

Indexed as

ApoptosisMesenchymal Stem CellsOxidative StressTumor Suppressor Protein p53AnimalsBone Marrow CellsCarrier ProteinsCells, CulturedFeedback, PhysiologicalHeat-Shock ProteinsHumansMicePhosphorylationUbiquitinationCarrier ProteinsHeat-Shock ProteinsTP53INP1 protein, humanTumor Suppressor Protein p53ApoptosisBone marrow mesenchymal stem cellsOxidative stressTumor protein p53 inducible nuclear protein 1Tumor suppressor p53

Identifiers

PMID38491252
PMCPMC11055765
OpenAlexW4394758508

What OpenQuestion holds

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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.