Evidence map›Paper›PMID 26105784›Full record

ArticleScientific reports2015

Heat stress induced apoptosis is triggered by transcription-independent p53, Ca(2+) dyshomeostasis and the subsequent Bax mitochondrial translocation.

Z T Gu, L Li, F Wu, P Zhao, H Yang, Y S Liu, Y Geng, M Zhao, L Su

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.

  1. Pooled it
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  20. Mitochondrial Permeability Transition in Stem Cells, Development, and Disease.Advances in experimental medicine and biology · 2023
    Review

6 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

9 authors at 4 institutions in 1 country.

Z T GuDepartment of intensive care unit, The Third Affiliated Hospital of Southern Medical University, Guangzhou, P.R. China; Department of Pathophysiology, Southern Medical University, Guangzhou 510515, P.R. China.
L LiDepartment of intensive care unit, The Third Affiliated Hospital of Southern Medical University, Guangzhou, P.R. China; Department of Pathophysiology, Southern Medical University, Guangzhou 510515, P.R. China.
F WuSouthern Medical University, Guangzhou, P.R. China.
P ZhaoDepartment of Gerontology, 421 Hospital of PLA, P.R. China.
H YangDepartment of intensive care unit, The Third Affiliated Hospital of Southern Medical University, Guangzhou, P.R. China; Department of Pathophysiology, Southern Medical University, Guangzhou 510515, P.R. China.
Y S LiuDepartment of intensive care unit, General Hospital of Guangzhou Military Command, Key Laboratory of Tropical Zone Trauma treatment and Tissue Repair of PLA, Guangzhou, PR China.
Y GengDepartment of intensive care unit, General Hospital of Guangzhou Military Command, Key Laboratory of Tropical Zone Trauma treatment and Tissue Repair of PLA, Guangzhou, PR China.
M ZhaoDepartment of Pathophysiology, Southern Medical University, Guangzhou 510515, P.R. China.
L SuDepartment of intensive care unit, General Hospital of Guangzhou Military Command, Key Laboratory of Tropical Zone Trauma treatment and Tissue Repair of PLA, Guangzhou, PR China.
General Hospital of Guangzhou Military Command · CNSouthern Medical University · CNThird Affiliated Hospital of Southern Medical University · CN421 Hospital of PLA · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, We demonstrated that Bax mitochondrial translocation plays a vital role in the initiation of the mitochondrial signaling pathway upon activation by heat stress. In addition, both p53 mitochondrial translocation and Ca(2+) signal mediated MPTP opening activate Bax mitochondrial translocation. Employing pifithrin-α (a p53 mitochondrial translocation inhibitor) and CsA (a permeability transition pore (MPTP) inhibitor), we found that heat stress induced Bax mitochondrial translocation was significantly inhibited in cells pretreated with both PFT and CsA. Furthermore, we demonstrated that generation of reactive oxygen species (ROS) is a critical mediator in heat stress induced apoptosis and that the antioxidant MnTBAP significantly decreased heat stress induced p53 mitochondrial translocation and Ca(2+) signal mediated MPTP opening, as well as the subsequent Bax mitochondrial translocation and activation of the caspase cascade. Taken together, our results indicate that heat stress induces apoptosis through the mitochondrial pathway with ROS dependent mitochondrial p53 translocation and Ca(2+) dyshomeostasis, and the ensuing intro Bax mitochondrial translocation as the upstream events involved in triggering the apoptotic process observed upon cellular exposure to heat stress.

Indexed as

HomeostasisTranscription, GeneticApoptosisbcl-2-Associated X ProteinCalciumCell DeathCell SurvivalHeat-Shock ResponseHumansHuman Umbilical Vein Endothelial CellsMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreProtein TransportReactive Oxygen SpeciesSignal Transductionbcl-2-Associated X ProteinCalciumMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreReactive Oxygen SpeciesTumor Suppressor Protein p53

Identifiers

PMID26105784
PMCPMC4478470
OpenAlexW2265677216

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.