Evidence map›Paper›PMID 36101496›Full record

ArticleDevelopment, growth & differentiation2022

A PI3Kγ signal regulates macrophage recruitment to injured tissue for regenerative cell survival.

Siyu Zhou, Zhengcheng Liu, Atsushi Kawakami

Open access · hybridAbstract read
In one paragraph

Article in Development, growth & differentiation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 43% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Engineering selective PI3KActa pharmaceutica Sinica. B · 2026
    Article
  2. Article
  3. 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.

Siyu ZhouSchool of Life Science and Technology, Tokyo Institute of Technology, Yokohama, Japan.
Zhengcheng LiuSchool of Life Science and Technology, Tokyo Institute of Technology, Yokohama, Japan.
Atsushi KawakamiSchool of Life Science and Technology, Tokyo Institute of Technology, Yokohama, Japan.ORCID https://orcid.org/0000-0001-9461-6372
Tokyo Institute of Technology · JP

Funding

Challenging Exploratory Research 19K22417Grant-in-Aid for Scientific Research (B) 19H03232
6 · The paper itself

Abstract

The interaction between immune cells and injured tissues is crucial for regeneration. Previous studies have shown that macrophages attenuate inflammation caused by injuries to support the survival of primed regenerative cells. Macrophage loss in zebrafish mutants like cloche (clo) causes extensive apoptosis in the regenerative cells of the amputated larval fin fold. However, the mechanism of interaction between macrophage and injured tissue is poorly understood. Here, we show that a phosphoinositide 3-kinase gamma (PI3Kγ)-mediated signal is essential for recruiting macrophages to the injured tissue. PI3Kγ inhibition by the PI3Kγ-specific inhibitor, 5-quinoxalin-6-ylmethylene-thiazolidine-2,4-dione (AS605240 or AS), displayed a similar apoptosis phenotype with that observed in clo mutants. We further show that PI3Kγ function during the early regenerative stage is necessary for macrophage recruitment to the injured site. Additionally, protein kinase B (Akt) overexpression in the AS-treated larvae suggested that Akt is not the direct downstream mediator of PI3Kγ for macrophage recruitment, while it independently plays a role for the survival of regenerative cells. Together, our study reveals that PI3Kγ plays a role for recruiting macrophages in response to regeneration.

Indexed as

Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAnimalsCell SurvivalMacrophagesPhosphatidylinositol 3-KinasePhosphoinositide-3 Kinase InhibitorsZebrafishPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktapoptosismacrophagePI3Kregenerationzebrafish

Identifiers

PMID36101496
PMCPMC9826243
OpenAlexW4295758312

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.