Evidence map›Paper›PMID 31078432›Full record

ReviewTrends in molecular medicine2019

Proteostasis and Beyond: ATF6 in Ischemic Disease.

Christopher C Glembotski, Jessica D Rosarda, R Luke Wiseman

Open access · greenAbstract readReview
In one paragraph

Review in Trends in molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
5.5field-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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
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  9. Growth hormone - releasing hormone in the immune system.Reviews in endocrine & metabolic disorders · 2025
    Review
  10. Article
  11. Endoplasmic reticulum stress in non-small cell lung cancer.American journal of cancer research · 2025
    Review
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7 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

3 authors at 2 institutions in 1 country.

Christopher C GlembotskiSan Diego State University Heart Institute and the Department of Biology, San Diego State University, San Diego, CA 92182, USA.
Jessica D RosardaDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA.
R Luke WisemanDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA. Electronic address: wiseman@scripps.edu.
Scripps Research Institute · USSan Diego State University · US

Funding

Establishing Strategies to Ameliorate Amyloid Pathology in Light Chain AmyloidosisR01DK107604 · NIDDK · SCRIPPS RESEARCH INSTITUTE, THE · PI WISEMAN, ROCKLAND LUKE · 2016 to 2024
$4.3M
Direct Regulation of Extracellular Proteostasis by the Unfolded Protein ResponseR01NS092829 · NINDS · SCRIPPS RESEARCH INSTITUTE, THE · PI WISEMAN, ROCKLAND LUKE · 2015 to 2019
$2.1M
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
The ER Stress-Induced Selenoprotein, SelenoS, Regulates Proteostasis and Cardiac HypertrophyR01HL149931 · NHLBI · UNIVERSITY OF ARIZONA · PI GLEMBOTSKI, CHRIS · 2020 to 2023
$1.7M
Harnessing the Adaptive ER Stress Response in Myocardial IschemiaR01HL135893 · NHLBI · UNIVERSITY OF ARIZONA · PI GLEMBOTSKI, CHRIS · 2017 to 2020
$1.5M
ATF6 is Required for ANP Secretion from the HeartR01HL141463 · NHLBI · UNIVERSITY OF ARIZONA · PI GLEMBOTSKI, CHRIS · 2019 to 2022
$1.5M
NHLBI NIH HHS R01 HL127439NHLBI NIH HHS R01 HL135893NHLBI NIH HHS R01 HL141463NHLBI NIH HHS R01 HL149931NIDDK NIH HHS R01 DK107604NINDS NIH HHS R01 NS092829
6 · The paper itself

Abstract

Endoplasmic reticulum (ER) stress is a pathological hallmark of numerous ischemic diseases, including stroke and myocardial infarction (MI). In these diseases, ER stress leads to activation of the unfolded protein response (UPR) and subsequent adaptation of cellular physiology in ways that dictate cellular fate following ischemia. Recent evidence highlights a protective role for the activating transcription factor 6 (ATF6) arm of the UPR in mitigating adverse outcomes associated with ischemia/reperfusion (I/R) injury in multiple disease models. This suggests ATF6 as a potential therapeutic target for intervening in diverse ischemia-related disorders. Here, we discuss the evidence demonstrating the importance of ATF6 signaling in protecting different tissues against ischemic damage and discuss preclinical results focused on defining the potential for pharmacologically targeting ATF6 to intervene in such diseases.

Indexed as

ProteostasisActivating Transcription Factor 6AnimalsBiomarkersDisease SusceptibilityEndoplasmic Reticulum StressHumansIschemiaMolecular Targeted TherapyMyocardial InfarctionOrgan SpecificitySignal TransductionUnfolded Protein ResponseActivating Transcription Factor 6ATF6 protein, humanBiomarkersATF6ER stressmyocardial infarctionstrokeunfolded protein response

Identifiers

PMID31078432
PMCPMC6592750
OpenAlexW2944292558

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.