Evidence map›Paper›PMID 36646692›Full record

ReviewCell death discovery2023

Regulatory T cell and macrophage crosstalk in acute lung injury: future perspectives.

Tianshu Guan, Xv Zhou, Wenwen Zhou, Hui Lin

Open access · goldAbstract readReview
In one paragraph

Review in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
13.3field-weighted citation impact, top 1% 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

55 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Advances in understanding mitophagy's role in lung injury.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2026
    Review
  3. Article
  4. Article
  5. Cleavage-Resistant CYLD Protects Against Autoimmune Hepatitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Regulation of inflammatory lung injury and repair by transforming growth factors.American journal of physiology. Lung cellular and molecular physiology · 2025
    Review
  17. Article
  18. 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 1 institution in 1 country.

Tianshu Guan *Department of Pathophysiology, School of Basic Medical Sciences, Nanchang University, 330006, Nanchang, Jiangxi, China.
Xv Zhou *Department of Pathophysiology, School of Basic Medical Sciences, Nanchang University, 330006, Nanchang, Jiangxi, China.
Wenwen ZhouDepartment of Pathophysiology, School of Basic Medical Sciences, Nanchang University, 330006, Nanchang, Jiangxi, China.
Hui LinDepartment of Pathophysiology, School of Basic Medical Sciences, Nanchang University, 330006, Nanchang, Jiangxi, China. huilin88@ncu.edu.cn.ORCID http://orcid.org/0000-0003-0343-1757
Nanchang University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31900852Natural Science Foundation of Jiangxi Province (Jiangxi Province Natural Science Foundation) 2018BAB215012Natural Science Foundation of Jiangxi Province (Jiangxi Province Natural Science Foundation) S2022ZRZDL0346
6 · The paper itself

Abstract

Acute lung injury (ALI) describes the injury to endothelial cells in the lungs and associated vessels due to various factors. Furthermore, ALI accompanied by inflammation and thrombosis has been reported as a common complication of SARS-COV-2 infection. It is widely accepted that inflammation and the cytokine storm are main causes of ALI. Two classical anti-inflammatory cell types, regulatory T cells (Tregs) and M2 macrophages, are theoretically capable of resisting uncontrolled inflammation. Recent studies have indicated possible crosstalk between Tregs and macrophages involving their mutual activation. In this review, we discuss the current findings related to ALI pathogenesis and the role of Tregs and macrophages. In particular, we review the molecular mechanisms underlying the crosstalk between Tregs and macrophages in ALI pathogenesis. Understanding the role of Tregs and macrophages will provide the potential targets for treating ALI.

Identifiers

PMID36646692
PMCPMC9841501
OpenAlexW4316466526

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.