Evidence map›Paper›PMID 20724307›Full record

ArticleCardiovascular research2011

Oestrogen prevents cardiomyocyte apoptosis by suppressing p38α-mediated activation of p53 and by down-regulating p53 inhibition on p38β.

Han Liu, Ali Pedram, Jin Kyung Kim

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardiovascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. The Role of P53 in Myocardial Ischemia-Reperfusion Injury.Cardiovascular drugs and therapy · 2025
    Review
  5. Article
  6. The interplay of hydrogen sulfide and microRNAs in cardiovascular diseases: insights and future perspectives.Mammalian genome : official journal of the International Mammalian Genome Society · 2024
    Review
  7. FemaleInternational journal of molecular sciences · 2024
    Article
  8. Article
  9. Implications for neutrophils in cardiac arrhythmias.American journal of physiology. Heart and circulatory physiology · 2024
    Review
  10. Review
  11. Article
  12. Article
  13. Role of estrogen receptors in health and disease.Frontiers in endocrinology · 2022
    Review
  14. Observational
  15. Article
  16. Review
  17. Article
  18. The Role of Estrogen Receptors in Cardiovascular Disease.International journal of molecular sciences · 2020
    Review
  19. 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

3 authors at 1 institution in 1 country.

Han LiuDepartment of Medicine, University of California-Irvine, Irvine, CA, USA.
Ali Pedram
Jin Kyung Kim
University of California, Irvine · US

Funding

Anti-apoptotic mechanisms of estrogen in cardiomyocytesK08HL089066 · NHLBI · UNIVERSITY OF CALIFORNIA-IRVINE · PI KIM, JIN KYUNG · 2007 to 2011
$638k
NHLBI NIH HHS K08 HL089066NHLBI NIH HHS K08HL089066
6 · The paper itself

Abstract

aimswe have previously shown that 17-β-estradiol (E2) protects cardiomyocytes exposed to simulated ischaemia-reperfusion (I/R) by differentially regulating pro-apoptotic p38α mitogen-activated protein kinase (p38α MAPK) and pro-survival p38β. However, little is known about how E2 modulation of these kinases alters apoptotic signalling. An attractive downstream target is p53, a well-known mediator of apoptosis and a substrate of p38α MAPK. The aim of this study was to determine whether the cytoprotective actions of oestrogen involve regulation of p53 via cardiac p38 MAPKs. METHODS AND

resultscultured rat cardiomyocytes underwent hypoxia followed by reoxygenation (H/R) to simulate I/R. We found that inhibiting p53 significantly reduced apoptosis. Phosphorylation of p53 at serine 15 [p-p53(S15)] increased after H/R in a p38α MAPK- and reactive oxygen species (ROS)-dependent manner. E2 at 10 nM effectively inhibited p-p53(S15) and mitochondrial translocation of p53. Blocking p53 led to augmented p38β activity and attenuated ROS, suggesting suppression of this antioxidant kinase by p53. The use of a specific agonist for each oestrogen receptor (ER) isoform, ERα and ERβ, demonstrated that both isoforms participate in preventing cell death by inhibiting p53 in the mitochondria-centred apoptotic processes.

conclusionour results demonstrate that during H/R stress, cardiomyocytes undergo p53-dependent apoptosis following phosphorylation of p53 by p38α MAPK, leading to p38β suppression. E2 protects cardiomyocytes by inhibiting p38α-p53 signalling in apoptosis.

Indexed as

AnimalsApoptosisCell HypoxiaCells, CulturedCell SurvivalDown-RegulationEnzyme ActivationEstradiolEstrogen Receptor alphaEstrogen Receptor betaFemaleHumansMaleMAP Kinase Signaling SystemMitogen-Activated Protein Kinase 11Mitogen-Activated Protein Kinase 14EstradiolEstrogen Receptor alphaEstrogen Receptor betaMitogen-Activated Protein Kinase 11Mitogen-Activated Protein Kinase 14Reactive Oxygen SpeciesTumor Suppressor Protein p53

Identifiers

PMID20724307
PMCPMC3002868
OpenAlexW2115404529

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.