Evidence map›Paper›PMID 24667845›Full record

ArticleScientific reports2014

Heat stress induces apoptosis through transcription-independent p53-mediated mitochondrial pathways in human umbilical vein endothelial cell.

Z T Gu, H Wang, L Li, Y S Liu, X B Deng, S F Huo, F F Yuan, Z F Liu, H S Tong, L Su

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
8.8field-weighted citation impact, top 1% 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

77 citing papers in PubMed, 154 citations in OpenAlex.

  1. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
    Article
  2. Review
  3. Article
  4. Oxidative Stress in Heat Stress Nephropathy: Crosstalk.Oxidative medicine and cellular longevity · 2026
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
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  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Inflammation, coagulation, and cellular injury in heat-induced shock.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  20. Article

17 more citing papers are in PubMed but not listed here.

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

10 authors at 2 institutions in 1 country.

Z T Gu1] The Key Laboratory of Molecular Biology, State Administration of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, P R China [2] Department of intensive care unit, General Hospital of Guangzhou Military Command, Key Laboratory of Tropical Zone Trauma Care and Tissue Repair of PLA, Guangzhou, PR China [3].
H Wang1] Department of Oncology, Cancer Research Institute, Southern Medical University, Guangzhou, PR China [2].
L Li1] The Key Laboratory of Molecular Biology, State Administration of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, P R China [2] Department of intensive care unit, General Hospital of Guangzhou Military Command, Key Laboratory of Tropical Zone Trauma Care and Tissue Repair of PLA, Guangzhou, PR China [3].
Y S LiuDepartment of intensive care unit, General Hospital of Guangzhou Military Command, Key Laboratory of Tropical Zone Trauma Care and Tissue Repair of PLA, Guangzhou, PR China.
X B DengDepartment of Oncology, Cancer Research Institute, Southern Medical University, Guangzhou, PR China.
S F HuoDepartment of Oncology, Cancer Research Institute, Southern Medical University, Guangzhou, PR China.
F F Yuan1] The Key Laboratory of Molecular Biology, State Administration of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, P R China [2] Department of intensive care unit, General Hospital of Guangzhou Military Command, Key Laboratory of Tropical Zone Trauma Care and Tissue Repair of PLA, Guangzhou, PR China.
Z F LiuDepartment of intensive care unit, General Hospital of Guangzhou Military Command, Key Laboratory of Tropical Zone Trauma Care and Tissue Repair of PLA, Guangzhou, PR China.
H S TongDepartment of intensive care unit, General Hospital of Guangzhou Military Command, Key Laboratory of Tropical Zone Trauma Care and Tissue Repair of PLA, Guangzhou, PR China.
L SuDepartment of intensive care unit, General Hospital of Guangzhou Military Command, Key Laboratory of Tropical Zone Trauma Care and Tissue Repair of PLA, Guangzhou, PR China.
General Hospital of Guangzhou Military Command · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cells apoptosis induced by intense heat stress is the prominent feature of heat-related illness. However, little is known about the biological effects of heat stress on cells apoptosis. Herein, we presented evidence that intense heat stress could induce early apoptosis of HUVEC cells through activating mitochondrial pathway with changes in mitochondrial membrane potential(ΔΨm), release of cytochrome c, and activation of caspase-9 and -3. We further revealed that p53 played a crucial role in heat stress-induced early apoptosis, with p53 protein rapidly translocated into mitochondria. Using pifithrin-α(PFT), a p53's mitochondrial translocation inhibitor, we found that pretreated with PFT, heat stress induced mitochondrial p53 translocation was significantly suppressed, accompanied by a significant alleviation in the loss of ΔΨm, cytochrome c release and caspase-9 activation. Furthermore, we also found that generation of reactive oxygen species (ROS) was a critical mediator in heat stress-induced apoptosis. In addition, the antioxidant MnTMPyP significantly decreased the heat stress-induced p53's mitochondrial translocation, followed by the loss of ΔΨm, cytochrome c release, caspase-9 activation and heat stress-mediated apoptosis. Conclusively, these findings indicate the contribution of the transcription-independent mitochondrial p53 pathway to early apoptosis in HUVEC cells induced by oxidative stress in response to intense heat stress.

Indexed as

Heat-Shock ResponseTranscription, GeneticApoptosisCaspasesCytochromes cHot TemperatureHumansHuman Umbilical Vein Endothelial CellsMembrane Potential, MitochondrialMitochondriaReactive Oxygen SpeciesSignal TransductionTumor Suppressor Protein p53CaspasesCytochromes cReactive Oxygen SpeciesTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID24667845
PMCPMC3966036
OpenAlexW2137218967

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.