Evidence map›Paper›PMID 36357527›Full record

ArticleInflammation2023

Inhibition of PD-1 Alters the SHP1/2-PI3K/Akt Axis to Decrease M1 Polarization of Alveolar Macrophages in Lung Ischemia-Reperfusion Injury.

Xiaojing He, Jingyuan Xiao, Zhao Li, Mengling Ye, Jinyuan Lin, Zhen Liu, Yubing Liang, Huijun Dai, Ren Jing, Fei Lin

Open access · hybridFull text read
In one paragraph

Article in Inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. LILRB4 Recruits SHP-1 to Enhance Oxidative Stress and Apoptosis, Aggravating Myocardial Ischemia-Reperfusion Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Advances in lung ischemia/reperfusion injury: unraveling the role of innate immunity.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Review
  10. Review
  11. Article
  12. 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

10 authors at 2 institutions in 1 country.

Xiaojing He *Department of Anesthesiology, Guangxi Medical University Cancer Hospital, Nanning, China.
Jingyuan Xiao *Department of Anesthesiology, Guangxi Medical University Cancer Hospital, Nanning, China.
Zhao LiDepartment of Experimental Research, Guangxi Medical University Cancer Hospital, Nanning, China.
Mengling YeDepartment of Experimental Research, Guangxi Medical University Cancer Hospital, Nanning, China.
Jinyuan LinDepartment of Anesthesiology, Guangxi Medical University Cancer Hospital, Nanning, China.
Zhen LiuDepartment of Anesthesiology, Guangxi Medical University Cancer Hospital, Nanning, China.
Yubing LiangDepartment of Anesthesiology, Guangxi Medical University Cancer Hospital, Nanning, China.
Huijun DaiDepartment of Anesthesiology, Guangxi Medical University Cancer Hospital, Nanning, China.
Ren JingDepartment of Anesthesiology, Guangxi Medical University Cancer Hospital, Nanning, China.
Fei LinDepartment of Anesthesiology, Guangxi Medical University Cancer Hospital, Nanning, China. linfei@gxmu.edu.cn.ORCID http://orcid.org/0000-0002-7497-6159
Guangxi Medical University · CNGuangxi University · CN

Funding

China Postdoctoral Science Foundation 2021M700911Guangxi Medical High-level Talents Program G201903011Guangxi Natural Science Fund General Project 2020GXNSFAA159123Guangxi Science and Technology Base and Talent Special Project AD22035047National Natural Science Foundation of China 81560018
6 · The paper itself

Abstract

Polarization of alveolar macrophages (AMs) into the M1 phenotype contributes to inflammatory responses and tissue damage that occur during lung ischemia-reperfusion injury (LIRI). Programmed cell death factor-1 (PD-1) regulates polarization of macrophages, but its role in LIRI is unknown. We examined the role of PD-1 in AM polarization in models of LIRI in vivo and in vitro. Adult Sprague-Dawley rats were subjected to ischemia-reperfusion with or without pretreatment with a PD-1 inhibitor, SHP1/2 inhibitor, or Akt activator. Lung tissue damage and infiltration by M1-type AMs were assessed. As an in vitro complement to the animal studies, rat alveolar macrophages in culture were subjected to oxygen/glucose deprivation and reoxygenation. Levels of SHP1/2 and Akt proteins were evaluated using Western blots, while levels of pro-inflammatory cytokines were measured using enzyme-linked immunosorbent assays. Injury upregulated PD-1 both in vivo and in vitro. Inhibiting PD-1 reduced the number of M1-type AMs, expression of SHP1 and SHP2, and levels of inflammatory cytokines. At the same time, it partially restored Akt activation. Similar results were observed after inhibition of SHP1/2 or activation of the PI3K/Akt pathway. PD-1 promotes polarization of AMs to the M1 phenotype and inflammatory responses through the SHP1/2-PI3K/Akt axis. Inhibiting PD-1 may be an effective therapeutic strategy to limit LIRI.

Indexed as

Macrophages, AlveolarReperfusion InjuryAnimalsCytokinesLungPhosphatidylinositol 3-KinasesProgrammed Cell Death 1 ReceptorProtein Tyrosine Phosphatase, Non-Receptor Type 6Proto-Oncogene Proteins c-aktRatsRats, Sprague-DawleyCytokinesPhosphatidylinositol 3-KinasesProgrammed Cell Death 1 ReceptorProtein Tyrosine Phosphatase, Non-Receptor Type 6Proto-Oncogene Proteins c-aktPTPN6 protein, humaninflammationlung ischemia–reperfusion injurymacrophage polarizationPD-1PI3K/Akt pathway.

Identifiers

PMID36357527
PMCPMC10024672
OpenAlexW4308770651

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read67
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.