Evidence map›Paper›PMID 27930699›Full record

ArticlePloS one2016

Estrogen Protects the Female Heart from Ischemia/Reperfusion Injury through Manganese Superoxide Dismutase Phosphorylation by Mitochondrial p38β at Threonine 79 and Serine 106.

Tao Luo, Han Liu, Jin Kyung Kim

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Mitochondrial Kinase Signaling for Cardioprotection.International journal of molecular sciences · 2024
    Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Sex-Related Effects on Cardiac Development and Disease.Journal of cardiovascular development and disease · 2022
    Review
  16. Review
  17. Oestrogenic Regulation of Mitochondrial Dynamics.International journal of molecular sciences · 2022
    Review
  18. Review
  19. Article
  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

3 authors at 1 institution in 1 country.

Tao LuoDivision of Cardiology, Department of Medicine, School of Medicine, University of California Irvine, Irvine, California, United States of America.
Han LiuDivision of Cardiology, Department of Medicine, School of Medicine, University of California Irvine, Irvine, California, United States of America.
Jin Kyung KimDivision of Cardiology, Department of Medicine, School of Medicine, University of California Irvine, Irvine, California, United States of America.
University of California, Irvine · US

Funding

Cardiomyocyte Apoptosis and Cardioprotective Actions of EstrogenR01HL111180 · NHLBI · UNIVERSITY OF CALIFORNIA-IRVINE · PI KIM, JIN KYUNG · 2013 to 2017
$1.9M
NHLBI NIH HHS R01 HL111180
6 · The paper itself

Abstract

A collective body of evidence indicates that estrogen protects the heart from myocardial ischemia/reperfusion (I/R) injury, but the underlying mechanism remains incompletely understood. We have previously delineated a novel mechanism of how 17β-estradiol (E2) protects cultured neonatal rat cardiomyocytes from hypoxia/reoxygenation (H/R) by identifying a functionally active mitochondrial pool of p38β and E2-driven upregulation of manganese superoxide dismutase (MnSOD) activity via p38β, leading to the suppression of reactive oxygen species (ROS) and apoptosis. Here we investigate these cytoprotective actions of E2 in vivo. Left coronary artery ligation and reperfusion was used to produce I/R injury in ovariectomized (OVX) female mice and in estrogen receptor (ER) null female mice. E2 treatment in OVX mice reduced the left ventricular infarct size accompanied by increased activity of mitochondrial p38β and MnSOD. I/R-induced infarct size in ERα knockout (ERKO), ERβ knockout (BERKO) and ERα and β double knockout (DERKO) female mice was larger than that in wild type (WT) mice, with little difference among ERKO, BERKO, and DERKO. Loss of both ERα and ERβ led to reduced activity of mitochondrial p38β and MnSOD at baseline and after I/R. The physical interaction between mitochondrial p38β and MnSOD in the heart was detected by co-immunoprecipitation (co-IP). Threonine 79 (T79) and serine 106 (S106) of MnSOD were identified to be phosphorylated by p38β in kinase assays. Overexpression of WT MnSOD in cardiomyocytes reduced ROS generation during H/R, while point mutation of T79 and S106 of MnSOD to alanine abolished its antioxidative function. We conclude that the protective effects of E2 and ER against cardiac I/R injury involve the regulation of MnSOD via posttranslational modification of the dismutase by p38β.

Indexed as

AnimalsEstradiolFemaleMitochondria, HeartMyocardial Reperfusion InjuryOvariectomyp38 Mitogen-Activated Protein KinasesPhosphorylationRatsRats, Sprague-DawleySerineSuperoxide DismutaseThreonineEstradiolp38 Mitogen-Activated Protein KinasesSerineSuperoxide DismutaseThreonine

Identifiers

PMID27930699
PMCPMC5145184
OpenAlexW2560399879

What Socratic 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 Socratic graph.