Evidence map›Paper›PMID 39101955›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2024

TRPV4 facilitates the reprogramming of inflamed macrophages by regulating IL-10 production via CREB.

Yassir Arfath, Tusharika Kotra, Md Imam Faizan, Areej Akhtar, Sheikh Tasduq Abdullah, Tanveer Ahmad, Zabeer Ahmed, Sheikh Rayees

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Phenotypic switching of gastrointestinal smooth muscle cells and the regulatory role of macrophages: a literature review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. 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

8 authors.

Yassir Arfath *Pharmacology Division, CSIR-Indian Institute of Integrative Medicine, Jammu, 180001, India.
Tusharika Kotra *Pharmacology Division, CSIR-Indian Institute of Integrative Medicine, Jammu, 180001, India.
Md Imam FaizanMultidisciplinary Centre for Advanced Research and Studies, JMI, New Delhi, 110025, India.
Areej AkhtarMultidisciplinary Centre for Advanced Research and Studies, JMI, New Delhi, 110025, India.
Sheikh Tasduq AbdullahPharmacology Division, CSIR-Indian Institute of Integrative Medicine, Jammu, 180001, India.
Tanveer AhmadMultidisciplinary Centre for Advanced Research and Studies, JMI, New Delhi, 110025, India.
Zabeer AhmedPharmacology Division, CSIR-Indian Institute of Integrative Medicine, Jammu, 180001, India. zahmed@iiim.res.in.
Sheikh RayeesPharmacology Division, CSIR-Indian Institute of Integrative Medicine, Jammu, 180001, India. rayees.sheikh@gmail.com.

Funding

Department of Biotechnology, Ramalingaswami Fellow grant BT/RLF/Re-entry/13/2019
6 · The paper itself

Abstract

backgroundTransient receptor potential vanilloid type 4 (TRPV4) is a versatile ion channel with diverse roles in immune cells, including macrophages. While its function in inflammation remains debated, we investigated its role in regulating IL-10 production and its impact on macrophage reprogramming during inflammation.

methodsWe investigated the connection between TRPV4 activation and CREB-mediated IL-10 production during inflammation. Notably, this signaling pathway was found to reprogram macrophages and enhance their ability to resist inflammatory damage. The experiments were conducted on primary macrophages and were further corroborated by animal studies.

resultsIn response to TRPV4 activation during inflammation, we observed a significant increase in intracellular Ca

conclusionOur study highlights the essential role of TRPV4 in regulating IL-10 production and mitochondrial health in macrophages during inflammation. These findings contribute to understand the role of TRPV4 in immune responses and suggest potential therapeutic targets for modulating inflammation-induced cellular dysfunction.

Indexed as

Cyclic AMP Response Element-Binding ProteinInflammationInterleukin-10MacrophagesMice, Inbred C57BLTRPV Cation ChannelsAnimalsCalciumCells, CulturedLipopolysaccharidesMaleMiceMitochondriaCalciumCreb1 protein, mouseCyclic AMP Response Element-Binding ProteinIL10 protein, mouseInterleukin-10LipopolysaccharidesTrpv4 protein, mouseTRPV Cation ChannelsCa2+CREBIL-10InflammationMitochondrial dysfunctionTRPV4

Identifiers

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.