Evidence map›Paper›PMID 36934284›Full record

ArticleImmunity & ageing : I & A2023

UGRP1-modulated MARCO

Yongyan Chen, Xiaolei Hao, Ming Li, Zhigang Tian, Min Cheng

Open access · goldFull text read
In one paragraph

Article in Immunity & ageing : I & A, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

13 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Single-Cell Insights Into Macrophage Subtypes in Pulmonary Infections.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Unveiling mechanisms of lung aging in COPD: A promising target for therapeutics development.Chinese medical journal pulmonary and critical care medicine · 2024
    Review
  10. Article
  11. Macrophage senescence in health and diseases.Acta pharmaceutica Sinica. B · 2024
    Review
  12. Macrophages in Lung Repair and Fibrosis.Results and problems in cell differentiation · 2024
    Review
  13. 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

5 authors at 3 institutions in 1 country.

Yongyan ChenHefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230027, China. yychen08@ustc.edu.cn.
Xiaolei HaoHefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230027, China.
Ming LiDepartment of Pathology, The Second Affiliated Hospital of Anhui Medical University, Hefei, 230601, Anhui, China.
Zhigang TianHefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230027, China.
Min ChengInstitute of Immunology, University of Science and Technology of China, Hefei, 230027, China. chengmin@ustc.edu.cn.
Anhui Provincial Hospital · CNUniversity of Science and Technology of China · CNSecond Affiliated Hospital of Anhui Medical University · CN

Funding

Anhui Provincial Key Research and Development Plan 2022e07020011National Natural Science Foundation of China 82171546Natural Science Foundation of Anhui Province 2008085MH277
6 · The paper itself

Abstract

The aging lungs are vulnerable to chronic pulmonary diseases; however, the underlying mechanisms are not well understood. In this study, we compared the aging lungs of 20-24-month-old mice with the young of 10-16-week-old mice, and found that aging airway epithelial cells significantly upregulated the expression of uteroglobin-related protein 1 (UGRP1), which was responsible for the higher levels of CCL6 in the aging lungs. Alveolar macrophages (AMs) changed intrinsically with aging, exhibiting a decrease in cell number and altered gene expression. Using terminal differentiation trajectories, a population of MARCO

Indexed as

Age-related lung fibrosisAlveolar macrophageCCL6MARCOUGRP1

Identifiers

PMID36934284
PMCPMC10024420
OpenAlexW4327723584

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read69
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.