Evidence map›Paper›PMID 30131723›Full record

ReviewFrontiers in physiology2018

Caveolae-Specific CaMKII Signaling in the Regulation of Voltage-Dependent Calcium Channel and Cardiac Hypertrophy.

Shota Tanaka, Yasushi Fujio, Hiroyuki Nakayama

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. CaPhysiological reviews · 2024
    Review
  4. Article
  5. Calcium and Heart Failure: How Did We Get Here and Where Are We Going?International journal of molecular sciences · 2021
    Review
  6. Article
  7. Article
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.

Shota TanakaLaboratory of Clinical Science and Biomedicine, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.
Yasushi FujioLaboratory of Clinical Science and Biomedicine, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.
Hiroyuki NakayamaLaboratory of Clinical Science and Biomedicine, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.
Osaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac hypertrophy is a major risk for the progression of heart failure; however, the underlying molecular mechanisms contributing to this process remain elusive. The caveolae microdomain plays pivotal roles in various cellular processes such as lipid homeostasis, signal transduction, and endocytosis, and also serves as a signaling platform. Although the caveolae microdomain has been postulated to have a major contribution to the development of cardiac pathologies, including cardiac hypertrophy, recent evidence has placed this role into question. Lack of direct evidence and appropriate methods for determining activation of caveolae-specific signaling has thus far limited the ability to obtain a definite answer to the question. In this review, we focus on the potential physiological and pathological roles of the multifunctional kinase Ca

Indexed as

CaMKIIcardiac hypertrophycaveolaecaveolinL-type calcium channel

Identifiers

PMID30131723
PMCPMC6090180
OpenAlexW2887192201

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.