Evidence map›Paper›PMID 34831084›Full record

ArticleCells2021

A-Kinase Anchoring Protein 2 Promotes Protection against Myocardial Infarction.

Darko Maric, Aleksandra Paterek, Marion Delaunay, Irene Pérez López, Miroslav Arambasic, Dario Diviani

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. LncRNAiScience · 2026
    Article
  3. Subcellular Stress Markers in Epithelial Ovarian Cancer.International journal of molecular sciences · 2025
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Lactylation-Boosted mResearch (Washington, D.C.) · 2025
    Article
  9. Review
  10. Review
  11. Cardiac-targeted delivery of a novel Drp1 inhibitor for acute cardioprotection.Journal of molecular and cellular cardiology plus · 2024
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. 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 2 institutions in 1 country.

Darko MaricDepartment of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, 1011 Lausanne, Switzerland.ORCID 0000-0001-8178-7746
Aleksandra PaterekDepartment of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, 1011 Lausanne, Switzerland.ORCID 0000-0002-6131-6004
Marion DelaunayDepartment of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, 1011 Lausanne, Switzerland.
Irene Pérez LópezDepartment of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, 1011 Lausanne, Switzerland.
Miroslav ArambasicDepartment of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, 1011 Lausanne, Switzerland.
Dario DivianiDepartment of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, 1011 Lausanne, Switzerland.ORCID 0000-0003-4375-3718
University of Lausanne · CHUniversity of Fribourg · CH

Funding

Swiss National Science Foundation 31003A_175838
6 · The paper itself

Abstract

Myocardial infarction (MI) is a leading cause of maladaptive cardiac remodeling and heart failure. In the damaged heart, loss of function is mainly due to cardiomyocyte death and remodeling of the cardiac tissue. The current study shows that A-kinase anchoring protein 2 (AKAP2) orchestrates cellular processes favoring cardioprotection in infarcted hearts. Induction of AKAP2 knockout (KO) in cardiomyocytes of adult mice increases infarct size and exacerbates cardiac dysfunction after MI, as visualized by increased left ventricular dilation and reduced fractional shortening and ejection fraction. In cardiomyocytes, AKAP2 forms a signaling complex with PKA and the steroid receptor co-activator 3 (Src3). Upon activation of cAMP signaling, the AKAP2/PKA/Src3 complex favors PKA-mediated phosphorylation and activation of estrogen receptor α (ERα). This results in the upregulation of ER-dependent genes involved in protection against apoptosis and angiogenesis, including Bcl2 and the vascular endothelial growth factor a (VEGFa). In line with these findings, cardiomyocyte-specific AKAP2 KO reduces Bcl2 and VEGFa expression, increases myocardial apoptosis and impairs the formation of new blood vessels in infarcted hearts. Collectively, our findings suggest that AKAP2 organizes a transcriptional complex that mediates pro-angiogenic and anti-apoptotic responses that protect infarcted hearts.

Indexed as

A Kinase Anchor ProteinsAnimalsAnimals, NewbornApoptosisCardiotonic AgentsCyclic AMP-Dependent Protein KinasesElectrocardiographyFibrosisGene DeletionMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutMyocardial InfarctionMyocardiumMyocytes, CardiacA Kinase Anchor ProteinsCardiotonic AgentsCyclic AMP-Dependent Protein KinasesGper1 protein, ratMembrane ProteinsNcoa3 protein, mouseNuclear Receptor Coactivator 3Pakap protein, mouseProto-Oncogene Proteins c-bcl-2Receptors, EstrogenReceptors, G-Protein-CoupledRNA, MessengerVascular Endothelial Growth Factor AA-kinase-anchoring protein (AKAP)cAMPcardiomyocytemyocardial infarctionprotein kinase Ascaffolding proteins

Identifiers

PMID34831084
PMCPMC8616452
OpenAlexW3208643001

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.