Evidence map›Paper›PMID 22001349›Full record

ArticleThe American journal of pathology2011

Heat shock protein 72 enhances autophagy as a protective mechanism in lipopolysaccharide-induced peritonitis in rats.

Shu Li, Yi Zhou, Jinjin Fan, Shirong Cao, Tao Cao, Fengxian Huang, Shougang Zhuang, Yihan Wang, Xueqing Yu, Haiping Mao

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Article
  3. Autophagy in peritoneal fibrosis.Frontiers in physiology · 2023
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Cell death and DAMPs in acute pancreatitis.Molecular medicine (Cambridge, Mass.) · 2014
    Review
  16. Management of a rapidly growing peritoneal dialysis population at the First Affiliated Hospital of Sun Yat-sen University.Peritoneal dialysis international : journal of the International Society for Peritoneal Dialysis · 2014
    Review
  17. Article
  18. Article
  19. Autophagy: An Integral Component of the Mammalian Stress Response.Journal of biochemical and pharmacological research · 2013
    Article
  20. It's a cell-eat-cell world: autophagy and phagocytosis.The American journal of pathology · 2013
    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

10 authors at 3 institutions in 2 countries.

Shu LiDepartment of Nephrology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Yi Zhou
Jinjin Fan
Shirong Cao
Tao Cao
Fengxian Huang
Shougang Zhuang
Yihan Wang
Xueqing Yu
Haiping Mao
Sun Yat-sen University · CNArkana Laboratories · USBrown University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Peritoneal dialysis-related peritonitis causes the denudation of mesothelial cells and, ultimately, membrane integrity alterations and peritoneal dysfunction. Because heat shock protein 72 (HSP72) confers protection against apoptosis and because autophagy mediates survival in response to cellular stresses, we examined whether autophagy contributes to HSP72-mediated cytoprotection in lipopolysaccharide (LPS)-induced peritonitis. Exposure of cultured peritoneal mesothelial cells to LPS resulted first in autophagy and later, apoptosis. Inhibition of autophagy by 3-methyladenine or Beclin-1 small-interfering RNA sensitized cells to apoptosis and abolished the antiapoptotic effect of HSP72, suggesting that autophagy activation acts as a prosurvival mechanism. Overexpression of HSP72 augmented autophagy through c-Jun N-terminal kinase (JNK) phosphorylation and Beclin-1 up-regulation. Suppression of JNK activity reversed HSP72-mediated Beclin-1 up-regulation and autophagy, indicating that HSP72-mediated autophagy is JNK dependent. In a rat model of LPS-associated peritonitis, autophagy occurred before apoptosis in peritoneum. Up-regulation of HSP72 by geranylgeranylacetone increased autophagy, inhibited apoptosis, and attenuated peritoneal injury, and these effects were blunted by down-regulation of HSP72 with quercetin. Additionally, blocking autophagy by chloroquine promoted apoptosis and aggravated LPS-associated peritoneal dysfunction. Thus, HSP72 protects peritoneum from LPS-induced mesothelial cells injury, at least in part by enhancing JNK activation-dependent autophagy and inhibiting apoptosis. These findings imply that HSP72 induction might be a potential therapy for peritonitis.

Indexed as

AdenineAnimalsApoptosisApoptosis Regulatory ProteinsAutophagyBeclin-1Cells, CulturedCell SurvivalChloroquineDiterpenesDose-Response Relationship, DrugEpithelial CellsGreen Fluorescent ProteinsHSP72 Heat-Shock ProteinsLipopolysaccharidesLuminescent Agents3-methyladenineAdenineApoptosis Regulatory ProteinsBeclin-1Becn1 protein, ratChloroquineDiterpenesgeranylgeranylacetoneGreen Fluorescent ProteinsHSP72 Heat-Shock ProteinsLipopolysaccharidesLuminescent AgentsRNA, Small Interfering

Identifiers

PMID22001349
PMCPMC3260826
OpenAlexW2021269700

What OpenQuestion holds

Textmetadata
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.