Evidence map›Paper›PMID 28038454›Full record

ArticleOncotarget2017

Reactive oxygen species mediate heat stress-induced apoptosis via ERK dephosphorylation and Bcl-2 ubiquitination in human umbilical vein endothelial cells.

Li Li, Hongping Tan, Hong Yang, Feng Li, Xuan He, Zhengtao Gu, Ming Zhao, Lei Su

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Thermal Cycling Stimulation via Nasal Inhalation Attenuates AβInternational journal of molecular sciences · 2025
    Article
  6. ZBP1 and heatstroke.Frontiers in immunology · 2023
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
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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 3 institutions in 1 country.

Li LiDepartment of Intensive Care Unit, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, P.R. China.
Hongping TanDepartment of Epilepsy Surgery, Guangdong Sanjiu Brain Hospital, Guangzhou 510510, P.R. China.
Hong YangDepartment of Intensive Care Unit, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, P.R. China.
Feng LiDepartment of Intensive Care Unit, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, P.R. China.
Xuan HeDepartment of Pathophysiology, Southern Medical University, Guangdong Provincial Key Laboratory of Shock and Microcirculation Research, Guangzhou 510515, P.R. China.
Zhengtao GuDepartment of Intensive Care Unit, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, P.R. China.
Ming ZhaoDepartment of Pathophysiology, Southern Medical University, Guangdong Provincial Key Laboratory of Shock and Microcirculation Research, Guangzhou 510515, P.R. China.
Lei SuSouthern Medical University, Guangzhou, 510515, China.
Southern Medical University · CNThird Affiliated Hospital of Southern Medical University · CNGuangdong 999 Brain Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heat stress can induce the mitochondrial apoptotic pathway in HUVEC cells, indicating that apoptosis may be a prominent pathological feature of heat stroke, however, little is known about the precise mechani sms involved in it. In this study, we describe the apoptotic effect of intense heat stress on HUVEC cells and our investigation of its underlying mechanisms. Treatment of cells with intense heat stress induced production of reactive oxygen species (ROS) and a concomitant increase in activation of the mitochondrial apoptotic pathway. Furthermore, by over-expression of MnSOD and GPx in cells, we show that ROS, and especially superoxide, is the primary oxidative species induced by intense heat stress and responsible for cell death. In addition, we explored the mechanism by which superoxide regulates the apoptotic effect of intense heat stress, and found that it involved Bcl-2 down-regulation through ubiquitin - proteasomal degradation. Superoxide production also led to Bcl-2 dephosphorylation through inactivation of MAP kinase ERK1/2, which promoted Bcl-2 ubiquitination. Taken together, these findings describe a novel pathway downstream of heat stress-induced apoptosis in HUVEC cells, and provide new insight into the process of redox-mediated down-regulation of Bcl-2 and apoptosis induction. These results could be important in the understanding of pathogenesis of heat stroke and for the development of preventive and treatment measures, both of which are currently lacking.

Indexed as

ApoptosisBlotting, WesternEndothelial CellsExtracellular Signal-Regulated MAP KinasesHeat-Shock ResponseHumansImmunoprecipitationPhosphorylationProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesUbiquitinationUmbilical VeinsExtracellular Signal-Regulated MAP KinasesProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesapoptosisBcl-2ERKheat stressreactive oxygen species

Identifiers

PMID28038454
PMCPMC5355065
OpenAlexW2565527757

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.