Evidence map›Paper›PMID 32676078›Full record

ReviewFrontiers in immunology2020

The Role of TRPV4 in Regulating Innate Immune Cell Function in Lung Inflammation.

Rachel G Scheraga, Brian D Southern, Lisa M Grove, Mitchell A Olman

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.1field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Focus on mechano-immunology: new direction in cancer treatment.International journal of surgery (London, England) · 2025
    Review
  9. TRPV4 facilitates the reprogramming of inflamed macrophages by regulating IL-10 production via CREB.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  10. Article
  11. TRPV4 Channel Modulators as Potential Drug Candidates for Cystic Fibrosis.International journal of molecular sciences · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Tuning immunity through tissue mechanotransduction.Nature reviews. Immunology · 2023
    Review
  16. Article
  17. Article
  18. TRPV4: A trigger of pathological RhoA activation in neurological disease.BioEssays : news and reviews in molecular, cellular and developmental biology · 2022
    Article
  19. Article
  20. 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

4 authors at 2 institutions in 1 country.

Rachel G ScheragaRespiratory Institute, Cleveland Clinic, Cleveland, OH, United States.
Brian D SouthernRespiratory Institute, Cleveland Clinic, Cleveland, OH, United States.
Lisa M GroveRespiratory Institute, Cleveland Clinic, Cleveland, OH, United States.
Mitchell A OlmanRespiratory Institute, Cleveland Clinic, Cleveland, OH, United States.
Cleveland Clinic · USCleveland Clinic Lerner College of Medicine · US

Funding

TRPV4-PI3K Axis Mediates Pulmonary and Cardiac FibrosisR01HL133721 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI OLMAN, MITCHELL ALAN, PRASAD, SATHYAMANGLA V · 2017 to 2020
$2.2M
Matrix-Myosin II Interactions Drive Fibrosis in Idiopathic Pulmonary Fibrosis.K08HL132079 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI SOUTHERN, BRIAN DERRIS · 2017 to 2021
$815k
Transient Receptor Potential Vanilloid 4 (TRPV4) mediates the host defense and lung injury response to bacterial pneumoniaK08HL133380 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI SCHERAGA, RACHEL GREENBERG · 2016 to 2020
$809k
NHLBI NIH HHS K08 HL132079NHLBI NIH HHS K08 HL133380NHLBI NIH HHS R01 HL133721
6 · The paper itself

Abstract

Ion channels/pumps are essential regulators of innate immune cell function. Macrophages have been increasingly recognized to have phenotypic plasticity and location-specific functions in the lung. Transient receptor potential vanilloid 4 (TRPV4) function in lung injury has been shown to be stimulus- and cell-type specific. In the current review, we discuss the importance of TRPV4 in macrophages and its role in phagocytosis and cytokine secretion in acute lung injury/acute respiratory distress syndrome (ARDS). Furthermore, TRPV4 controls a MAPK molecular switch from predominately c-Jun N-terminal kinase, JNK activation, to that of p38 activation, that mediates phagocytosis and cytokine secretion in a matrix stiffness-dependent manner. Expanding knowledge regarding the downstream mechanisms by which TRPV4 acts to tailor macrophage function in pulmonary inflammatory diseases will allow for formulation of novel therapeutics.

Indexed as

Disease SusceptibilityImmunity, InnateImmunomodulationAnimalsCell PlasticityHumansMacrophagesPneumoniaSignal TransductionTRPV Cation ChannelsTRPV4 protein, humanTRPV Cation Channelsinnate immunitylung inflammation and injurymacrophageMAPKTRPV4 (transient receptor potential vanilloid-4)

Identifiers

PMID32676078
PMCPMC7333351
OpenAlexW3037600314

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.