Evidence map›Paper›PMID 23850759›Full record

ReviewBiochimica et biophysica acta2013

ER stress-induced cell death mechanisms.

Renata Sano, John C Reed

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,052 papers.

0numbers the graph read from it
0cells of the map it votes in
1,052citing papers in PubMed
54.6field-weighted citation impact, top 1% 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

1,052 citing papers in PubMed, 1,978 citations in OpenAlex.

  1. Article
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  7. Review
  8. Article
  9. Beneficially Stressing the Peripheral Nervous System to Repair.International journal of molecular sciences · 2026
    Review
  10. Article
  11. Article
  12. The influence of exercise duration on inhibiting endoplasmic reticulum stress in ischemic stroke rats.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
    Article
  13. Cell surface GRP78 and the UPR pathway as novel promising therapeutic targets in cancer: an insight into the treatment of acute leukemia by using GRP78-CART cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  14. Article
  15. Cytotoxic Effects of Cnidarian Venoms: One Cancer, Two Cell Lines.Marine biotechnology (New York, N.Y.) · 2026
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

992 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

2 authors at 1 institution in 1 country.

Renata SanoSanford-Burnham Medical Research Institute, La Jolla, CA, 92037, USA.
John C ReedSanford-Burnham Medical Research Institute, La Jolla, CA, 92037, USA. Electronic address: reedoffice@sanfordburnham.org.
Sanford Burnham Prebys Medical Discovery Institute · US

Funding

BI-1, Regulator ER-Stress Pathways Linked to ApoptosisR01AG015393 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI REED, JOHN C · 1998 to 2009
$2.8M
NIA NIH HHS AG-15393NIA NIH HHS R01 AG015393
6 · The paper itself

Abstract

The endoplasmic-reticulum (ER) stress response constitutes a cellular process that is triggered by a variety of conditions that disturb folding of proteins in the ER. Eukaryotic cells have developed an evolutionarily conserved adaptive mechanism, the unfolded protein response (UPR), which aims to clear unfolded proteins and restore ER homeostasis. In cases where ER stress cannot be reversed, cellular functions deteriorate, often leading to cell death. Accumulating evidence implicates ER stress-induced cellular dysfunction and cell death as major contributors to many diseases, making modulators of ER stress pathways potentially attractive targets for therapeutics discovery. Here, we summarize recent advances in understanding the diversity of molecular mechanisms that govern ER stress signaling in health and disease. This article is part of a Special Section entitled: Cell Death Pathways.

Indexed as

Endoplasmic Reticulum StressAnimalsCell DeathDiseaseHumansModels, BiologicalSignal TransductionUnfolded Protein Responseactivating transcription factor 4activating transcription factor 6advanced glycated end-productsAGEage-related macular degenerationALSAMDamyotropic lateral sclerosisantioxidant response elementsapoptotic-signaling kinase-1AREASK1ATF4ATF6ATF/cAMP response elementsBAGBARbax-inhibitor 1Bcl-2 associated athanogeneBI-1bifunctional apoptosis regulatorbinding immunoglobulin proteinBiPcalcium-sensing receptorCASRCell death mechanismsCHOPCMVCREcytomegalovirusDiseasesDRP-1dynamin-related proteinelF2αendoplasmic reticulumendoplasmic reticulum oxidoreductase-1ERERADER antigen peptide transporter 1ER-assisted degradationERO1αERSEER StressER stress-response elementeukaryotic translation initiation factorGADD34growth arrest and DNA damage-inducible 34HCVheme oxygenase 1hepatitis C virusherpes simplex virusHFDhigh fat dietHO-1HSVIBDIECinflammatory bowel diseaseinositol-requiring protein-1inositol triphosphate receptorintestinal epithelial cellsIP(3)RIRE1αJNKJun-N-terminal kinasemajor histocompatibility complexMEFMHCmouse embryonic fibroblastNLRPNOD-like receptor, (NLR) family pyrin domain-containingNRF2nuclear erythroid 2 p45-related factor 2PDIA6PERKPKCprotein disulfide isomerase associated 6protein kinase Cprotein kinase RNA (PKR)-like ER kinaseregulated IRE1-dependent decay of mRNAretinitis pigmentosaRIDDRPsingle nucleotide polymorphismSNPT2DMTAP1thioredoxin-interacting proteinTLRtoll-like receptortranscriptional factor C/EBP homologous proteinTXNIPtype 2 diabetesunfolded protein responseUPRvascular endothelial growth factorVEGFX box-binding protein-1XBP-1

Identifiers

PMID23850759
PMCPMC3834229
OpenAlexW2085933321

What OpenQuestion holds

Textmetadata
LicenceTDM
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.