Evidence map›Paper›PMID 33666503›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2021

The peroxisomal enzyme, FAR1, is induced during ER stress in an ATF6-dependent manner in cardiac myocytes.

Kayleigh G Marsh, Adrian Arrieta, Donna J Thuerauf, Erik A Blackwood, Lauren MacDonnell, Christopher C Glembotski

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. The peroxisome: an update on mysteries 3.0.Histochemistry and cell biology · 2024
    Review
  7. Article
  8. Review
  9. 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

6 authors at 3 institutions in 1 country.

Kayleigh G MarshSan Diego State University Heart Institute and Department of Biology, San Diego State University, San Diego, California.
Adrian ArrietaSan Diego State University Heart Institute and Department of Biology, San Diego State University, San Diego, California.ORCID 0000-0002-1875-5714
Donna J ThueraufSan Diego State University Heart Institute and Department of Biology, San Diego State University, San Diego, California.
Erik A BlackwoodSan Diego State University Heart Institute and Department of Biology, San Diego State University, San Diego, California.ORCID 0000-0003-0912-4133
Lauren MacDonnellSan Diego State University Heart Institute and Department of Biology, San Diego State University, San Diego, California.
Christopher C GlembotskiSan Diego State University Heart Institute and Department of Biology, San Diego State University, San Diego, California.
University of Arizona · USSan Diego State University · USUniversity of California, Los Angeles · US

Funding

Non-canonical ERAD as a Regulator of Cardiac HypertrophyR01HL157027 · NHLBI · UNIVERSITY OF ARIZONA · PI GLEMBOTSKI, CHRIS · 2022 to 2025
$2.6M
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
The Adaptive Cardiac Sensor, ATF6, Regulates ANP Secretion and Decreases Hypertensive StressF31HL140850 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI BLACKWOOD, ERIK · 2018 to 2020
$69k
NHLBI NIH HHS F31 HL140850NHLBI NIH HHS R01 HL135893NHLBI NIH HHS R01 HL141463NHLBI NIH HHS R01 HL149931NHLBI NIH HHS R01 HL157027
6 · The paper itself

Abstract

Although peroxisomes have been extensively studied in other cell types, their presence and function have gone virtually unexamined in cardiac myocytes. Here, in neonatal rat ventricular myocytes (NRVM) we showed that several known peroxisomal proteins co-localize to punctate structures with a morphology typical of peroxisomes. Surprisingly, we found that the peroxisomal protein, fatty acyl-CoA reductase 1 (FAR1), was upregulated by pharmacological and pathophysiological ER stress induced by tunicamycin (TM) and simulated ischemia-reperfusion (sI/R), respectively. Moreover, FAR1 induction in NRVM was mediated by the ER stress sensor, activating transcription factor 6 (ATF6). Functionally, FAR1 knockdown reduced myocyte death during oxidative stress induced by either sI/R or hydrogen peroxide (H

Indexed as

Endoplasmic Reticulum StressActivating Transcription Factor 6Aldehyde OxidoreductasesAnimalsAnimals, NewbornCell HypoxiaCells, CulturedCell SurvivalEnzyme InductionHydrogen PeroxideMyocardial Reperfusion InjuryMyocytes, CardiacOxidative StressPeroxisomesRatsTunicamycinActivating Transcription Factor 6Aldehyde OxidoreductasesAtf6 protein, ratFar1 protein, ratHydrogen PeroxideTunicamycinATF6cardiomyocyteFAR1ischemia-reperfusionperoxisome

Identifiers

PMID33666503
PMCPMC8163642
OpenAlexW3133967044

What OpenQuestion holds

Textmetadata
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.