Evidence map›Paper›PMID 25120434›Full record

ReviewFrontiers in cellular neuroscience2014

A molecular web: endoplasmic reticulum stress, inflammation, and oxidative stress.

Namrata Chaudhari, Priti Talwar, Avinash Parimisetty, Christian Lefebvre d'Hellencourt, Palaniyandi Ravanan

Abstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 292 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
292citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

292 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. BPTF is essential for vaccine-induced germinal center B cell responses.Journal of immunology (Baltimore, Md. : 1950) · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. Article

232 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

5 authors.

Namrata ChaudhariApoptosis and Cell Death Research Lab, School of Biosciences and Technology, Vellore Institute of Technology University , Vellore , India.
Priti TalwarApoptosis and Cell Death Research Lab, School of Biosciences and Technology, Vellore Institute of Technology University , Vellore , India.
Avinash ParimisettyGroupe d'Etude sur l'Inflammation Chronique et l'Obésité, EA 41516, Plateforme CYROI, Université de La Réunion , Saint Denis de La Réunion , France.
Christian Lefebvre d'HellencourtGroupe d'Etude sur l'Inflammation Chronique et l'Obésité, EA 41516, Plateforme CYROI, Université de La Réunion , Saint Denis de La Réunion , France.
Palaniyandi RavananApoptosis and Cell Death Research Lab, School of Biosciences and Technology, Vellore Institute of Technology University , Vellore , India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Execution of fundamental cellular functions demands regulated protein folding homeostasis. Endoplasmic reticulum (ER) is an active organelle existing to implement this function by folding and modifying secretory and membrane proteins. Loss of protein folding homeostasis is central to various diseases and budding evidences suggest ER stress as being a major contributor in the development or pathology of a diseased state besides other cellular stresses. The trigger for diseases may be diverse but, inflammation and/or ER stress may be basic mechanisms increasing the severity or complicating the condition of the disease. Chronic ER stress and activation of the unfolded-protein response (UPR) through endogenous or exogenous insults may result in impaired calcium and redox homeostasis, oxidative stress via protein overload thereby also influencing vital mitochondrial functions. Calcium released from the ER augments the production of mitochondrial Reactive Oxygen Species (ROS). Toxic accumulation of ROS within ER and mitochondria disturbs fundamental organelle functions. Sustained ER stress is known to potentially elicit inflammatory responses via UPR pathways. Additionally, ROS generated through inflammation or mitochondrial dysfunction could accelerate ER malfunction. Dysfunctional UPR pathways have been associated with a wide range of diseases including several neurodegenerative diseases, stroke, metabolic disorders, cancer, inflammatory disease, diabetes mellitus, cardiovascular disease, and others. In this review, we have discussed the UPR signaling pathways, and networking between ER stress-induced inflammatory pathways, oxidative stress, and mitochondrial signaling events, which further induce or exacerbate ER stress.

Indexed as

calciumendoplasmic reticulum stressinflammationIRE1αNF-κBoxidative stress

Identifiers

PMID25120434
PMCPMC4114208

What OpenQuestion holds

Textmetadata
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.