Evidence map›Paper›PMID 21547407›Full record

ReviewEuropean journal of nutrition2011

Inflammation and cellular stress: a mechanistic link between immune-mediated and metabolically driven pathologies.

Eva Rath, Dirk Haller

Abstract readReview
PubMed Publisher
In one paragraph

Review in European journal of nutrition, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

35 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Regulation of Oxygen Homeostasis at the Intestinal Epithelial Barrier Site.International journal of molecular sciences · 2021
    Review
  5. Article
  6. Article
  7. Review
  8. Mitochondrial function - gatekeeper of intestinal epithelial cell homeostasis.Nature reviews. Gastroenterology & hepatology · 2018
    Review
  9. Article
  10. Article
  11. Review
  12. The cellular autophagy/apoptosis checkpoint during inflammation.Cellular and molecular life sciences : CMLS · 2017
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Mitochondrial dysfunction in inflammatory bowel disease.Frontiers in cell and developmental biology · 2015
    Review
  18. Review
  19. Article
  20. Article
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

2 authors at 1 institution in 1 country.

Eva RathChair for Biofunctionality, ZIEL-Research Center for Nutrition and Food Science, CDD-Center for Diet and Disease, Technische Universität München, Gregor-Mendel-Str. 2, 85350, Freising-Weihenstephan, Germany.
Dirk Haller
Technical University of Munich · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMultiple cellular stress responses have been implicated in chronic diseases such as obesity, diabetes, cardiovascular, and inflammatory bowel diseases. Even though phenotypically different, chronic diseases share cellular stress signaling pathways, in particular endoplasmic reticulum (ER) unfolded protein response (UPR). RESULTS AND

methodsThe purpose of the ER UPR is to restore ER homeostasis after challenges of the ER function. Among the triggers of ER UPR are changes in the redox status, elevated protein synthesis, accumulation of unfolded or misfolded proteins, energy deficiency and glucose deprivation, cholesterol depletion, and microbial signals. Numerous mouse models have been used to characterize the contribution of ER UPR to several pathologies, and ER UPR-associated signaling has also been demonstrated to be relevant in humans. Additionally, recent evidence suggests that the ER UPR is interrelated with metabolic and inflammatory pathways, autophagy, apoptosis, and mitochondrial stress signaling. Furthermore, microbial as well as nutrient sensing is integrated into the ER-associated signaling network.

conclusionThe data discussed in the present review highlight the interaction of ER UPR with inflammatory pathways, metabolic processes and mitochondrial function, and their interrelation in the context of chronic diseases.

Indexed as

Stress, PhysiologicalUnfolded Protein ResponseActivating Transcription Factor 6AnimalsAutophagyeIF-2 KinaseEndoplasmic ReticulumEndoribonucleasesHomeostasisHumansInflammationMetabolic DiseasesMitochondriaMolecular Targeted TherapyOxidative StressProtein Serine-Threonine KinasesActivating Transcription Factor 6eIF-2 KinaseEndoribonucleasesERN1 protein, humanProtein Serine-Threonine Kinases

Identifiers

PMID21547407
OpenAlexW2012757056

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.