Evidence map›Paper›PMID 37762367›Full record

ReviewInternational journal of molecular sciences2023

Unfolded Protein Response Signaling in Liver Disorders: A 2023 Updated Review.

Smriti Shreya, Christophe F Grosset, Buddhi Prakash Jain

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. [Protective effect of the endoplasmic reticulum stress inhibitor 4-phenylbutyric acid against myocardial injury in septic mice].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
    Article
  3. Mitochondrial Calcium Signaling in Hepatocyte Health and Disease.Cold Spring Harbor perspectives in biology · 2026
    Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. ATF6 Alleviates Endothelial Inflammation Following Extended Hepatectomy Through Inhibition of TRIM10/NF-κB Signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. 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

3 authors at 2 institutions in 2 countries.

Smriti ShreyaGene Expression and Signaling Lab, Department of Zoology, Mahatma Gandhi Central University, Motihari 845401, Bihar, India.
Christophe F GrossetMIRCADE Team, U1312, Bordeaux Institute in Oncology, BRIC, Université de Bordeaux, 146 Rue Léo Saignat, F-33000 Bordeaux, France.ORCID 0000-0002-0479-6291
Buddhi Prakash JainGene Expression and Signaling Lab, Department of Zoology, Mahatma Gandhi Central University, Motihari 845401, Bihar, India.ORCID 0000-0002-7225-7257
Central University of South Bihar · INUniversité de Bordeaux · FR

Funding

Foundation for Addie's ResearchGroupama Centre-AtlantiqueInstitut National du Cancer (INCa) N°2020-012, 2021-169, 2023-018La Fondation Groupama pour la SantéLa Région Nouvelle-Aquitaine N°2018-1R30114, 2019-1R3M0102, AAPR2020A-2019-8100110, AAPR2022-2021-17296410
6 · The paper itself

Abstract

Endoplasmic reticulum (ER) is the site for synthesis and folding of secreted and transmembrane proteins. Disturbance in the functioning of ER leads to the accumulation of unfolded and misfolded proteins, which finally activate the unfolded protein response (UPR) signaling. The three branches of UPR-IRE1 (Inositol requiring enzyme 1), PERK (Protein kinase RNA-activated (PKR)-like ER kinase), and ATF6 (Activating transcription factor 6)-modulate the gene expression pattern through increased expression of chaperones and restore ER homeostasis by enhancing ER protein folding capacity. The liver is a central organ which performs a variety of functions which help in maintaining the overall well-being of our body. The liver plays many roles in cellular physiology, blood homeostasis, and detoxification, and is the main site at which protein synthesis occurs. Disturbance in ER homeostasis is triggered by calcium level imbalance, change in redox status, viral infection, and so on. ER dysfunction and subsequent UPR signaling participate in various hepatic disorders like metabolic (dysfunction) associated fatty liver disease, liver cancer, viral hepatitis, and cholestasis. The exact role of ER stress and UPR signaling in various liver diseases is not fully understood and needs further investigation. Targeting UPR signaling with drugs is the subject of intensive research for therapeutic use in liver diseases. The present review summarizes the role of UPR signaling in liver disorders and describes why UPR regulators are promising therapeutic targets.

Indexed as

Liver NeoplasmsUnfolded Protein ResponseEndoplasmic Reticulum StressHumansMolecular ChaperonesSignal TransductionMolecular Chaperonesendoplasmic reticulumhepatocellular carcinomaliver disordersnon-alcoholic fatty liver diseaseunfolded protein response

Identifiers

PMID37762367
PMCPMC10531763
OpenAlexW4386747306

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.