Evidence map›Paper›PMID 26482920›Full record

ReviewSeminars in immunopathology2016

"TRP inflammation" relationship in cardiovascular system.

Tomohiro Numata, Kiriko Takahashi, Ryuji Inoue

Open access · hybridAbstract readReview
In one paragraph

Review in Seminars in immunopathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 26% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Oxidative Stress and Hypertension.Circulation research · 2021
    Review
  8. Article
  9. Article
  10. Implications of immune-inflammatory responses in smooth muscle dysfunction and disease.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Significant contribution of TRPC6 channel-mediated CaJournal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2016
    Review
  15. 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

3 authors at 1 institution in 1 country.

Tomohiro NumataDepartment of Physiology, Graduate School of Medical Sciences, Fukuoka University, Nanakuma 7-45-1, Johnan-ku, Fukuoka, 814-0180, Japan. numata@fukuoka-u.ac.jp.
Kiriko TakahashiDepartment of Physiology, Graduate School of Medical Sciences, Fukuoka University, Nanakuma 7-45-1, Johnan-ku, Fukuoka, 814-0180, Japan.
Ryuji InoueDepartment of Physiology, Graduate School of Medical Sciences, Fukuoka University, Nanakuma 7-45-1, Johnan-ku, Fukuoka, 814-0180, Japan. inouery@fukuoka-u.ac.jp.
Fukuoka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite considerable advances in the research and treatment, the precise relationship between inflammation and cardiovascular (CV) disease remains incompletely understood. Therefore, understanding the immunoinflammatory processes underlying the initiation, progression, and exacerbation of many cardiovascular diseases is of prime importance. The innate immune system has an ancient origin and is well conserved across species. Its activation occurs in response to pathogens or tissue injury. Recent studies suggest that altered ionic balance, and production of noxious gaseous mediators link to immune and inflammatory responses with altered ion channel expression and function. Among plausible candidates for this are transient receptor potential (TRP) channels that function as polymodal sensors and scaffolding proteins involved in many physiological and pathological processes. In this review, we will first focus on the relevance of TRP channel to both exogenous and endogenous factors related to innate immune response and transcription factors related to sustained inflammatory status. The emerging role of inflammasome to regulate innate immunity and its possible connection to TRP channels will also be discussed. Secondly, we will discuss about the linkage of TRP channels to inflammatory CV diseases, from a viewpoint of inflammation in a general sense which is not restricted to the innate immunity. These knowledge may serve to provide new insights into the pathogenesis of various inflammatory CV diseases and their novel therapeutic strategies.

Indexed as

AnimalsCardiovascular DiseasesCardiovascular SystemDisease SusceptibilityHost-Pathogen InteractionsHumansImmunity, InnateImmunomodulationInflammasomesInflammationInflammation MediatorsReactive Oxygen SpeciesSignal TransductionTransient Receptor Potential ChannelsInflammasomesInflammation MediatorsReactive Oxygen SpeciesTransient Receptor Potential ChannelsCardiovascularDiseaseInflammasomeInflammationInnate immune systemTRP

Identifiers

PMID26482920
PMCPMC4851701
OpenAlexW2157663736

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.