Evidence map›Paper›PMID 38594728›Full record

ArticleCell communication and signaling : CCS2024

Atg5 deficiency in macrophages protects against kidney fibrosis via the CCR6-CCL20 axis.

Yufeng Zhu, Jiexing Tan, Yuanzhan Wang, Yuhong Gong, Xiaoyong Zhang, Ziguo Yuan, Xinyu Lu, Huifang Tang, Zhiming Zhang, Xiaotao Jiang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2024. 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
3.9field-weighted citation impact, top 6% 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, 10 citations in OpenAlex.

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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

12 authors at 5 institutions in 1 country.

Yufeng Zhu *Experimental Animal Center, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Baiyun District, Guangzhou, 510515, China.
Jiexing Tan *Experimental Animal Center, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Baiyun District, Guangzhou, 510515, China.
Yuanzhan Wang *Experimental Animal Center, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Baiyun District, Guangzhou, 510515, China.
Yuhong GongExperimental Animal Center, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Baiyun District, Guangzhou, 510515, China.
Xiaoyong ZhangState Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Viral Hepatitis Research, Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Ziguo YuanCollege of Veterinary Medicine, South China Agricultural University, Guangzhou, China.
Xinyu LuDepartment of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Huifang TangDepartment of Pharmacology, School of Basic Medical Sciences, Zhejiang University, Hangzhou, China.
Zhiming ZhangDepartment of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Xiaotao Jiang *Department of Immunology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Wei Zhu *Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Li Gong *Experimental Animal Center, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Baiyun District, Guangzhou, 510515, China. gongli009@126.com.
Nanfang Hospital · CNSouthern Medical University · CNKey Laboratory of Guangdong Province · CNSouth China Agricultural University · CNZhejiang University · CN

Funding

Guangdong Science and Technology Program Project 2017A030303022National Natural Science Foundation of Chin 31572342Natural Science Foundation of Guangdong Province 2020A1515010981Science and Technology Program of Guangzhou 202102080193The Nanfang Hospital Dean Fund 2020NF0016
6 · The paper itself

Abstract

backgroundAutophagy is a lysosome-dependent degradation pathway that regulates macrophage activation, differentiation, and polarization. Autophagy related 5 (Atg5) is a key protein involved in phagocytic membrane elongation in autophagic vesicles that forms a complex with Atg12 and Atg16L1. Alterations in Atg5 are related to both acute and chronic kidney diseases in experimental models. However, the role of macrophage-expressed Atg5 in acute kidney injury remains unclear.

methodsUsing a myeloid cell-specific Atg5 knockout (MΦ atg5

resultsBased on changes in the serum urea nitrogen and creatinine levels, Atg5 deletion had a minimal effect on renal function in the early stages after mild injury; however, MΦ atg5

conclusionsOur data indicate that Atg5 deficiency decreased macrophage migration by impairing the CCL20-CCR6 axis and inhibited M2 polarization, thereby improving kidney fibrosis.

Indexed as

Ureteral ObstructionAnimalsAutophagy-Related Protein 5Chemokine CCL20FibrosisIschemiaKidneyMacrophagesMiceMice, Inbred C57BLReceptors, CCR6Atg5 protein, mouseAutophagy-Related Protein 5CCL20 protein, mouseCCR6 protein, mouseChemokine CCL20Receptors, CCR6Acute kidney injuryAutophagyAutophagy-related 5MacrophageRenal fibrosis

Identifiers

PMID38594728
PMCPMC11003172
OpenAlexW4394621634

What OpenQuestion holds

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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.