Evidence map›Paper›PMID 17537920›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2007

The A-kinase anchoring protein (AKAP)-Lbc-signaling complex mediates alpha1 adrenergic receptor-induced cardiomyocyte hypertrophy.

Aline Appert-Collin, Susanna Cotecchia, Monique Nenniger-Tosato, Thierry Pedrazzini, Dario Diviani

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

66 citing papers in PubMed, 103 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Signalling of Adrenoceptors: Canonical Pathways and New Paradigms.Handbook of experimental pharmacology · 2024
    Review
  8. Article
  9. Bactericidal and Antiviral Bionic Metalized Nanocoatings.Nanomaterials (Basel, Switzerland) · 2022
    Article
  10. Article
  11. GPCRs thatSmall GTPases · 2022
    Review
  12. Article
  13. RhoA: a dubious molecule in cardiac pathophysiology.Journal of biomedical science · 2021
    Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Review

6 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Aline Appert-CollinDépartement de Pharmacologie et de Toxicologie, Faculté de Biologie et de Médecine, Université de Lausanne, Rue du Bugnon 27, 1005 Lausanne, Switzerland.
Susanna Cotecchia
Monique Nenniger-Tosato
Thierry Pedrazzini
Dario Diviani
University of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In response to various pathological stresses, the heart undergoes a pathological remodeling process that is associated with cardiomyocyte hypertrophy. Because cardiac hypertrophy can progress to heart failure, a major cause of lethality worldwide, the intracellular signaling pathways that control cardiomyocyte growth have been the subject of intensive investigation. It has been known for more than a decade that the small molecular weight GTPase RhoA is involved in the signaling pathways leading to cardiomyocyte hypertrophy. Although some of the hypertrophic pathways activated by RhoA have now been identified, the identity of the exchange factors that modulate its activity in cardiomyocytes is currently unknown. In this study, we show that AKAP-Lbc, an A-kinase anchoring protein (AKAP) with an intrinsic Rho-specific guanine nucleotide exchange factor activity, is critical for activating RhoA and transducing hypertrophic signals downstream of alpha1-adrenergic receptors (ARs). In particular, our results indicate that suppression of AKAP-Lbc expression by infecting rat neonatal ventricular cardiomyocytes with lentiviruses encoding AKAP-Lbc-specific short hairpin RNAs strongly reduces both alpha1-AR-mediated RhoA activation and hypertrophic responses. Interestingly, alpha1-ARs promote AKAP-Lbc activation via a pathway that requires the alpha subunit of the heterotrimeric G protein G12. These findings identify AKAP-Lbc as the first Rho-guanine nucleotide exchange factor (GEF) involved in the signaling pathways leading to cardiomyocytes hypertrophy.

Indexed as

Signal TransductionAdaptor Proteins, Signal TransducingA Kinase Anchor ProteinsAnimalsAnimals, NewbornCell LineCells, CulturedHeart VentriclesHumansHypertrophyMyocytes, CardiacRatsReceptors, Adrenergic, alpha-1Adaptor Proteins, Signal TransducingAkap1 protein, ratA Kinase Anchor ProteinsReceptors, Adrenergic, alpha-1

Identifiers

PMID17537920
PMCPMC1891209
OpenAlexW2011008275

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.