Evidence map›Paper›PMID 29026925›Full record

ReviewCurrent topics in microbiology and immunology

ER Protein Quality Control and the Unfolded Protein Response in the Heart.

A Arrieta, E A Blackwood, C C Glembotski

Abstract readReview
In one paragraph

Review in Current topics in microbiology and immunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
9.1field-weighted citation impact, top 2% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Ion channel trafficking implications in heart failure.Frontiers in cardiovascular medicine · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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 1 institution in 1 country.

A ArrietaSan Diego State University Heart Institute and the Department of Biology, San Diego State University, San Diego, CA, 92182, USA.
E A BlackwoodSan Diego State University Heart Institute and the Department of Biology, San Diego State University, San Diego, CA, 92182, USA.
C C GlembotskiSan Diego State University Heart Institute and the Department of Biology, San Diego State University, San Diego, CA, 92182, USA. cglembotski@mail.sdsu.edu.
San Diego State University · US

Funding

Role of Unfolded Protein Response in Cardiac ProtectionR01HL075573 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI GLEMBOTSKI, CHRIS · 2004 to 2011
$3.0M
Role of the SR/ER E3 Ubiquitin Ligase Synoviolin 1 in Cardiac HypertrophyR01HL127439 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI GLEMBOTSKI, CHRIS · 2015 to 2018
$1.7M
Harnessing the Adaptive ER Stress Response in Myocardial IschemiaR01HL135893 · NHLBI · UNIVERSITY OF ARIZONA · PI GLEMBOTSKI, CHRIS · 2017 to 2020
$1.5M
NHLBI NIH HHS R01 HL075573NHLBI NIH HHS R01 HL127439NHLBI NIH HHS R01 HL135893
6 · The paper itself

Abstract

Cardiac myocytes are the cells responsible for the robust ability of the heart to pump blood throughout the circulatory system. Cardiac myocytes grow in response to a variety of physiological and pathological conditions; this growth challenges endoplasmic reticulum-protein quality control (ER-PQC), a major feature of which includes the unfolded protein response (UPR). ER-PQC and the UPR in cardiac myocytes growing under physiological conditions, including normal development, exercise, and pregnancy, are sufficient to support hypertrophic growth of each cardiac myocyte. However, the ER-PQC and UPR are insufficient to respond to the challenge of cardiac myocyte growth under pathological conditions, including myocardial infarction and heart failure. In part, this insufficiency is due to a continual decline in the expression levels of important adaptive UPR components as a function of age and during myocardial pathology. This chapter will discuss the physiological and pathological conditions unique to the heart that involves ER-PQC, and whether the UPR is adaptive or maladaptive under these circumstances.

Indexed as

Activating Transcription Factor 6AnimalseIF-2 KinaseEndoplasmic ReticulumHumansMyocardiumMyocytes, CardiacProteinsUnfolded Protein ResponseActivating Transcription Factor 6ATF6 protein, humanEIF2AK3 protein, humaneIF-2 KinaseProteins

Identifiers

PMID29026925
PMCPMC6459409
OpenAlexW2761142123

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.