Evidence map›Paper›PMID 38125505›Full record

ArticleHeliyon2023

Heat stress suppresses MnSOD expression via p53-Sp1 interaction and induces oxidative stress damage in endothelial cells: Protective effects of MitoQ10 and Pifithrin-α.

Jian Gong, Peipei Sun, Li Li, Zhimin Zou, Qihua Wu, Liyun Sun, Hui Li, Zhengtao Gu, Lei Su

Open access · goldAbstract read
In one paragraph

Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

  1. Ferroptosis in heatstroke: Mechanisms and therapeutic perspectives (Review).International journal of molecular medicine · 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 3 institutions in 1 country.

Jian GongDepartment of Critical Care Medicine, The First School of Clinical Medicine, Southern Medical University (General Hospital of Southern Theater Command of PLA), Guangzhou, 510515, China.
Peipei SunDepartment of Intensive Care Medicine, The Third People's Hospital of Longgang District, Shenzhen, 518115, China.
Li LiDepartment of Treatment Center for Traumatic Injuries, The Third Affiliated Hospital of Southern Medical University, Guangzhou, 510630, China.
Zhimin ZouDepartment of Treatment Center for Traumatic Injuries, The Third Affiliated Hospital of Southern Medical University, Guangzhou, 510630, China.
Qihua WuDepartment of Intensive Care Medicine, The Third People's Hospital of Longgang District, Shenzhen, 518115, China.
Liyun SunDepartment of Intensive Care Medicine, The Third People's Hospital of Longgang District, Shenzhen, 518115, China.
Hui LiDepartment of Critical Care Medicine, The First School of Clinical Medicine, Southern Medical University (General Hospital of Southern Theater Command of PLA), Guangzhou, 510515, China.
Zhengtao GuDepartment of Treatment Center for Traumatic Injuries, The Third Affiliated Hospital of Southern Medical University, Guangzhou, 510630, China.
Lei SuDepartment of Critical Care Medicine, The First School of Clinical Medicine, Southern Medical University (General Hospital of Southern Theater Command of PLA), Guangzhou, 510515, China.
Longgang Central Hospital · CNThird Affiliated Hospital of Southern Medical University · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aim: To investigate the mechanism of p53-mediated suppression of heat stress-induced oxidative stress damage by manganese superoxide dismutase (MnSOD) in endothelial cells (ECs). Methods: Primary ECs isolated from mouse aortas were used to examine the effects of heat stress on vascular ECs viability and apoptosis. We measured MnSOD expression, reactive oxygen species (ROS) production, p53 expression, viability, and apoptosis of heat stress-induced ECs. We also tested the protective effects of MitoQ10, a mitochondrial-targeted antioxidant, and Pifithrin-α, a p53 inhibitor, in ECs from a mouse model of heat stroke. Results: Heat stress increased cellular apoptosis, ROS production, and p53 expression, while reducing cellular viability and MnSOD expression in ECs. We also showed that the suppression of MnSOD expression by heat stress in ECs was mediated by interactions between p53 and Sp1. Furthermore, MitoQ10 and Pifithrin-α alleviated heat stress-induced oxidative stress and apoptosis in ECs. Conclusion: Our results revealed that p53-mediated MnSOD downregulation is a key mechanism for heat stress-induced oxidative stress damage in ECs and indicated that MitoQ10 and Pifithrin-α could be potential therapeutic agents for heat stroke.

Indexed as

Endothelial cellsHeat stressManganese superoxide dismutaseOxidative stressp53

Identifiers

PMID38125505
PMCPMC10730713
OpenAlexW4388967827

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.