Evidence map›Paper›PMID 31817027›Full record

ReviewCancers2019

ER Stress and Unfolded Protein Response in Cancer Cachexia.

Anirban Roy, Ashok Kumar

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 59 citations in OpenAlex.

  1. Trial
  2. TAK1 Regulates Skeletal Muscle Mass, Hypertrophic Signaling, and Metabolic Homeostasis in Male and Female Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
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  10. UBR2 targets myosin heavy chain IIb and IIx for degradation: Molecular mechanism essential for cancer-induced muscle wasting.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  11. Article
  12. c-MYC-mediated TRIB3/P62Acta pharmaceutica Sinica. B · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  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.

Anirban RoyDepartment of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USA.
Ashok KumarDepartment of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USA.
University of Houston · US

Funding

TAK1/TRAF6 Signaling in Skeletal MuscleR01AR059810 · NIAMS · UNIVERSITY OF LOUISVILLE · PI KUMAR, ASHOK · 2011 to 2021
$4.0M
MYD88 Signaling in Mammalian Myoblast FusionR01AR068313 · NIAMS · UNIVERSITY OF LOUISVILLE · PI KUMAR, ASHOK · 2015 to 2019
$1.7M
NIAMS NIH HHS AR059810NIAMS NIH HHS AR068313NIAMS NIH HHS R01 AR059810NIAMS NIH HHS R01 AR068313
6 · The paper itself

Abstract

Cancer cachexia is a devastating syndrome characterized by unintentional weight loss attributed to extensive skeletal muscle wasting. The pathogenesis of cachexia is multifactorial because of complex interactions of tumor and host factors. The irreversible wasting syndrome has been ascribed to systemic inflammation, insulin resistance, dysfunctional mitochondria, oxidative stress, and heightened activation of ubiquitin-proteasome system and macroautophagy. Accumulating evidence suggests that deviant regulation of an array of signaling pathways engenders cancer cachexia where the human body is sustained in an incessant self-consuming catabolic state. Recent studies have further suggested that several components of endoplasmic reticulum (ER) stress-induced unfolded protein response (UPR) are activated in skeletal muscle of animal models and muscle biopsies of cachectic cancer patients. However, the exact role of ER stress and the individual arms of the UPR in the regulation of skeletal muscle mass in various catabolic states including cancer has just begun to be elucidated. This review provides a succinct overview of emerging roles of ER stress and the UPR in cancer-induced skeletal muscle wasting.

Indexed as

and signaling.ATF4ATF6cancer cachexiaER stressIRE1PERKSkeletal muscleXBP1

Identifiers

PMID31817027
PMCPMC6966641
OpenAlexW2992521468

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.