Evidence map›Paper›PMID 24567387›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

MURC/Cavin-4 facilitates recruitment of ERK to caveolae and concentric cardiac hypertrophy induced by α1-adrenergic receptors.

Takehiro Ogata, Daisuke Naito, Naohiko Nakanishi, Yukiko K Hayashi, Takuya Taniguchi, Kotaro Miyagawa, Tetsuro Hamaoka, Naoki Maruyama, Satoaki Matoba, Koji Ikeda and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

43 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
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  6. YTHDF1 is pivotal for maintenance of cardiac homeostasis.Journal of molecular and cellular cardiology · 2024
    Article
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  8. Article
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  11. ERK1/2 in immune signalling.Biochemical Society transactions · 2022
    Review
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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

13 authors at 3 institutions in 1 country.

Takehiro OgataDepartment of Cardiovascular Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Daisuke Naito
Naohiko Nakanishi
Yukiko K Hayashi
Takuya Taniguchi
Kotaro Miyagawa
Tetsuro Hamaoka
Naoki Maruyama
Satoaki Matoba
Koji Ikeda
Hiroyuki Yamada
Hidemasa Oh
Tomomi Ueyama
Kyoto Prefectural University of Medicine · JPOkayama University Hospital · JPTokyo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The actions of catecholamines on adrenergic receptors (ARs) induce sympathetic responses, and sustained activation of the sympathetic nervous system results in disrupted circulatory homeostasis. In cardiomyocytes, α1-ARs localize to flask-shaped membrane microdomains known as "caveolae." Caveolae require both caveolin and cavin proteins for their biogenesis and function. However, the functional roles and molecular interactions of caveolar components in cardiomyocytes are poorly understood. Here, we showed that muscle-restricted coiled-coil protein (MURC)/Cavin-4 regulated α1-AR-induced cardiomyocyte hypertrophy through enhancement of ERK1/2 activation in caveolae. MURC/Cavin-4 was expressed in the caveolae and T tubules of cardiomyocytes. MURC/Cavin-4 overexpression distended the caveolae, whereas MURC/Cavin-4 was not essential for their formation. MURC/Cavin-4 deficiency attenuated cardiac hypertrophy induced by α1-AR stimulation in the presence of caveolae. Interestingly, MURC/Cavin-4 bound to α1A- and α1B-ARs as well as ERK1/2 in caveolae, and spatiotemporally modulated MEK/ERK signaling in response to α1-AR stimulation. Thus, MURC/Cavin-4 facilitates ERK1/2 recruitment to caveolae and efficient α1-AR signaling mediated by caveolae in cardiomyocytes, which provides a unique insight into the molecular mechanisms underlying caveola-mediated signaling in cardiac hypertrophy.

Indexed as

AnimalsBlotting, WesternCardiomegalyCaveolaeDNA PrimersEchocardiographyImmunoprecipitationMAP Kinase Signaling SystemMiceMice, Inbred C57BLMice, KnockoutMicroscopy, Electron, TransmissionMicroscopy, FluorescenceMuscle ProteinsMyocytes, CardiacRatsCavin4 protein, mouseDNA PrimersMuscle ProteinsReceptors, Adrenergic, alpha-1caveolaheartplasma membranesignal transduction

Identifiers

PMID24567387
PMCPMC3956167
OpenAlexW2062457718

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.