Evidence map›Paper›PMID 27995459›Full record

ArticleThe journal of physiological sciences : JPS2018

Epac activation inhibits IL-6-induced cardiac myocyte dysfunction.

Huiling Jin, Takayuki Fujita, Meihua Jin, Reiko Kurotani, Yuko Hidaka, Wenqian Cai, Kenji Suita, Rajesh Prajapati, Chen Liang, Yoshiki Ohnuki and 6 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in The journal of physiological sciences : JPS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Review
  6. Review
  7. Interleukin-6-Mediated-CaFrontiers in immunology · 2021
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 4 institutions in 1 country.

Huiling JinCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Takayuki FujitaCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Meihua JinCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Reiko KurotaniCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Yuko HidakaCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Wenqian CaiCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Kenji SuitaCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Rajesh PrajapatiCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Chen LiangCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Yoshiki OhnukiDepartment of Physiology, Tsurumi University School of Dental Medicine, 2-1-3 Tsurumi, Tsurumi-ku, Yokohama, 230-8501, Japan.
Yasumasa MototaniDepartment of Physiology, Tsurumi University School of Dental Medicine, 2-1-3 Tsurumi, Tsurumi-ku, Yokohama, 230-8501, Japan.
Masanari UmemuraCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Utako YokoyamaCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Motohiko SatoCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.
Satoshi OkumuraCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan. okumura-s@tsurumi-u.ac.jp.
Yoshihiro IshikawaCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan. yishikaw@yokohama-cu.ac.jp.
Yokohama City University · JPTsurumi University · JPNational Cerebral and Cardiovascular Center · JPYamagata University · JP

Funding

Grant for Strategic Research Promotion of Yokohama City University S2501Japan Agency for Medical Research and Development 66890001Japan Agency for Medical Research and Development 66890005Japan Agency for Medical Research and Development 66890011Japan Agency for Medical Research and Development 66890023Japan Society for the Promotion of Science 16H05300Japan Society for the Promotion of Science 16K08501Japan Society for the Promotion of Science 16K15205Japan Society for the Promotion of Science 23591087Japan Society for the Promotion of Science 25460296Ministry of Education, Culture, Sports, Science, and Technology 22136009Ministry of Education, Culture, Sports, Science, and Technology S1511018
6 · The paper itself

Abstract

Pro-inflammatory cytokines are released in septic shock and impair cardiac function via the Jak-STAT pathway. It is well known that sympathetic and thus catecholamine signaling is activated thereafter to compensate for cardiac dysfunction. The mechanism of such compensation by catecholamine signaling has been traditionally understood to be cyclic AMP-dependent protein kinase (PKA)-mediated enforcement of cardiac contractility. We hypothesized that the exchange protein activated by cAMP (Epac), a newly identified target of cAMP signaling that functions independently of PKA, also plays a key role in this mechanism. In cultured cardiac myocytes, activation of Epac attenuated the inhibitory effect of interleukin-6 on the increase of intracellular Ca

Indexed as

AnimalsCyclic AMPCyclic AMP-Dependent Protein KinasesGuanine Nucleotide Exchange FactorsHeart FailureInterleukin-6Janus KinasesMyocytes, CardiacNitric Oxide Synthase Type IIPhosphorylationRatsSignal TransductionSTAT Transcription FactorsSuppressor of Cytokine Signaling 3 ProteinCyclic AMPCyclic AMP-Dependent Protein KinasesGuanine Nucleotide Exchange FactorsInterleukin-6Janus KinasesNitric Oxide Synthase Type IIRapgef3 protein, ratSTAT Transcription FactorsSuppressor of Cytokine Signaling 3 ProteincAMPCatecholamineContractilityCytokineEpacJak-STAT

Identifiers

PMID27995459
PMCPMC6353818
OpenAlexW2560915885

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.