Evidence map›Paper›PMID 30838215›Full record

ArticleFrontiers in cardiovascular medicine2019

Cardiac Specific Knockout of p53 Decreases ER Stress-Induced Mitochondrial Damage.

Qun Chen, Jeremy Thompson, Ying Hu, Anindita Das, Edward J Lesnefsky

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cardiovascular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

26 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  8. Endoplasmic reticulum stress and mitochondrial dysfunction during aging: Role of sphingolipids.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2023
    Article
  9. Review
  10. Article
  11. Review
  12. The Role of Oxidative Stress in the Aging Heart.Antioxidants (Basel, Switzerland) · 2022
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. The regulatory roles of p53 in cardiovascular health and disease.Cellular and molecular life sciences : CMLS · 2021
    Review
  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

5 authors at 2 institutions in 1 country.

Qun ChenDivision of Cardiology, Departments of Medicine, Virginia Commonwealth University, Richmond, VA, United States.
Jeremy ThompsonDivision of Cardiology, Departments of Medicine, Virginia Commonwealth University, Richmond, VA, United States.
Ying HuDivision of Cardiology, Departments of Medicine, Virginia Commonwealth University, Richmond, VA, United States.
Anindita DasDivision of Cardiology, Departments of Medicine, Virginia Commonwealth University, Richmond, VA, United States.
Edward J LesnefskyDivision of Cardiology, Departments of Medicine, Virginia Commonwealth University, Richmond, VA, United States.
Virginia Commonwealth University · USHunter Holmes McGuire VA Medical Center · US

Funding

Cardioprotection with mTOR InhibitionR01HL134366 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI DAS, ANINDITA, KUKREJA, RAKESH C · 2016 to 2019
$2.1M
activation of mitochondrial calpain augments cardiac injury in aged heartsR21AG054975 · NIA · VIRGINIA COMMONWEALTH UNIVERSITY · PI CHEN, QUN · 2017 to 2018
$433k
Reduction of cardiac injury by targeting damaged mitochondria during reperfusionI01BX001355 · VA · VA VETERANS ADMINISTRATION HOSPITAL · PI LESNEFSKY, EDWARD J · 2012 to 2025
–
BLRD VA I01 BX001355NHLBI NIH HHS R01 HL134366NIA NIH HHS R21 AG054975
6 · The paper itself

Abstract

Endoplasmic reticulum (ER) stress contributes to cardiovascular disease including heart failure. Interactions between the ER and mitochondria during ER stress can impair the mitochondrial respiratory chain and increase cell injury. p53 is a tumor suppressor protein that regulates apoptosis. p53 contributes to the regulation of mitochondrial and ER interactions, especially during the progression of ER stress. The knockout (KO) of p53 leads to decreased injury in hearts following ischemia-reperfusion. We asked if KO of p53 can protect mitochondria during the induction of ER stress and decrease cell injury. Floxed p53 mice were crossed with mice carrying an α-myosin heavy chain

Indexed as

apoptosiscomplex Imitochondriapyruvate dehydrogenasethapsigargin

Identifiers

PMID30838215
PMCPMC6389610
OpenAlexW2916725045

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.