Evidence map›Paper›PMID 28380464›Full record

ArticleOncotarget2017

Heat stress induces intestinal injury through lysosome- and mitochondria-dependent pathway in vivo and in vitro.

Gao Yi, Li Li, Meijuan Luo, Xuan He, Zhimin Zou, Zhengtao Gu, 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 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 65 citations in OpenAlex.

  1. The role of lysosome-dependent cell death in cancer.Apoptosis : an international journal on programmed cell death · 2026
    Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Inflammation, coagulation, and cellular injury in heat-induced shock.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  10. Article
  11. Article
  12. ZBP1 and heatstroke.Frontiers in immunology · 2023
    Review
  13. Review
  14. Review
  15. Article
  16. Duodenal Metabolic Profile Changes in Heat-Stressed Broilers.Animals : an open access journal from MDPI · 2022
    Article
  17. Article
  18. Burn Injury: Mechanisms of Keratinocyte Cell Death.Medical sciences (Basel, Switzerland) · 2021
    Review
  19. Article
  20. Review
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

7 authors at 3 institutions in 1 country.

Gao YiSouthern Medical University, Guangzhou, 510515, P.R. China.
Li LiDepartment of Intensive Care Unit, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, P.R. China.
Meijuan LuoDepartment of Pediatrics, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, 510180, P.R. China.
Xuan HeSouthern Medical University, Guangzhou, 510515, P.R. China.
Zhimin ZouSouthern Medical University, Guangzhou, 510515, P.R. China.
Zhengtao GuDepartment of Intensive Care Unit, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, P.R. China.
Lei SuSouthern Medical University, Guangzhou, 510515, P.R. China.
Southern Medical University · CNGuangzhou First People's Hospital · CNThird Affiliated Hospital of Southern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Damage to the small intestine secondary to heat stroke is a major factor in heat stroke-related morbidity and mortality. However, the underlying mechanisms by which heat stroke causes small intestinal lesions and dysfunction remain unclear. To explore the pathogenesis of small intestinal tissue and epithelial cell injury, the SW480 cell heat stress model and the mice heat stroke model were established to mimic heat stroke. Morphologic changes in intestinal tissue and increased TUNEL-positive index were induced by heat stress in vivo. Heat stress activated the lysosomal-mitochondrial apoptotic pathway in SW480 cells, increasing intracellular reactive oxygen species and causing lysosomal membrane permeabilization with subsequent release of cathepsin B to the cytosol, mitochondrial depolarization, and cytochrome C release to cytosol. An increase in the Bax/Bcl2 ratio, caspase-9 and caspase-3 were observed. N-Acetyl-L-Cysteine was shown to inhibit ROS generation, suppress permeabilization of lysosomal membranes, decrease levels of cathepsin B and cytochrome C in the cytosol, and inhibit Bax/Bcl2 ratio, caspase-9 and caspase-3 activity both in vitro and in vivo. Mitochondrial damage was alleviated when the models were pre-treated with CA-074 Me both in vitro and in vivo, decreasing cathepsin B and cytochrome C levels in the cytosol, Bax/Bcl2 ratio, caspase-9 and caspase-3 activity. In our models, heat stress-induced apoptosis of small intestinal tissue and epithelial cells through accumulation of ROS and activation of the lysosomal-mitochondrial apoptotic pathway involved the release of cathepsin B. These findings may offer potentially pharmaceutical targets and strategies to repair intestinal injury caused by heat stroke.

Indexed as

AnimalsApoptosisCathepsin BCell Line, TumorHeat Stress DisordersHot TemperatureHumansIntestinal DiseasesIntestinal MucosaIntestinesIntestine, SmallLysosomesMaleMiceMice, Inbred BALB CMitochondriaCathepsin BReactive Oxygen Speciesapoptosiscathepsin Bheat stresslysosomal membrane permeabilizationmitochondrial

Identifiers

PMID28380464
PMCPMC5522251
OpenAlexW2598826952

What OpenQuestion holds

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LicenceCC BY
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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.