Evidence map›Paper›PMID 36436910›Full record

ArticleExperimental animals2023

Impaired healing of cutaneous wound in a Trpv1 deficient mouse.

Kazuki Ueno, Shizuya Saika, Yuka Okada, Hiroki Iwanishi, Kentaro Suzuki, Gen Yamada, Shinichi Asamura

Open access · diamondAbstract read
In one paragraph

Article in Experimental animals, 2023. 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
1.2field-weighted citation impact, top 20% 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, 12 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. TRP Ion Channels in Immune Cells and Their Implications for Inflammation.International journal of molecular sciences · 2024
    Review
  7. 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

7 authors at 2 institutions in 1 country.

Kazuki UenoDepartment of Plastic and Reconstructive Surgery, Wakayama Medical University, 811-1 Kimiidera, Wakayama 641-8509, Japan.
Shizuya SaikaDepartment of Ophthalmology, Wakayama Medical University, 811-1 Kimiidera, Wakayama 641-8509, Japan.
Yuka OkadaDepartment of Ophthalmology, Wakayama Medical University, 811-1 Kimiidera, Wakayama 641-8509, Japan.
Hiroki IwanishiDepartment of Ophthalmology, Wakayama Medical University, 811-1 Kimiidera, Wakayama 641-8509, Japan.
Kentaro SuzukiDepartment of Developmental Genetics, Institute of Advanced Medicine, Wakayama Medical University, 811-1 Kimiidera, Wakayama 641-8509, Japan.
Gen YamadaDepartment of Plastic and Reconstructive Surgery, Wakayama Medical University, 811-1 Kimiidera, Wakayama 641-8509, Japan.
Shinichi AsamuraDepartment of Plastic and Reconstructive Surgery, Wakayama Medical University, 811-1 Kimiidera, Wakayama 641-8509, Japan.
Wakayama Medical University · JPTakeda (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transient Receptor Potential (TRP) ion channels mediate the influx of cations into cells responding to chemical or physical stimuli. TRP vanilloid 1 (TRPV1) regulates cutaneous functions. Its function in cutaneous wound healing, however, has not been clarified. The current study elucidated the role of TRPV1 in cutaneous wound healing of dorsal circular excisional injury using Trpv1-null (KO) and wild type (WT) male/female C57BL/6 mice. Macroscopic observation showed that the remaining cutaneous lesion was significantly larger in KO than that of WT at postoperative days (POD) 7 and 10. Histological analysis showed significantly delayed re-epithelialization in KO at POD7. The number of macrophages in KO and WT similarly returned to the reduced state from POD4 to POD7. Whereas, the number of neutrophils in KO did not significantly return to the reduced state, in contrast to WT. Of note, The H3Cit-labeled NETs (Neutrophil Extracellular Traps) formation of KO was prominently increased both in POD4 and 7. The current results suggest that the loss of TRPV1 induces prolonged neutrophilic inflammation and NETs formation, retarding murine cutaneous wound healing in vivo. This study provides a possible link with TRPV1 and neutrophilic regulation in cutaneous wound healing.

Indexed as

TRPV Cation ChannelsWound HealingAnimalsFemaleMaleMiceMice, Inbred C57BLMice, KnockoutTRPV1 protein, mouseTRPV Cation Channelsknockout mouseneutrophilNeutrophil Extracellular Traps (NETs)transient receptor potential vanilloid subtype 1 (TRPV1)wound healing

Identifiers

PMID36436910
PMCPMC10202716
OpenAlexW4310336299

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.