Evidence map›Paper›PMID 39844180›Full record

ArticleCell communication and signaling : CCS2025

Atg5 deficiency in basophils improves metabolism in lupus mice by regulating gut microbiota dysbiosis.

Jiaxuan Chen, Quanren Pan, Lu Lu, Xiaorong Huang, Shuting Wang, Xiaoxian Liu, Jiaqi Lun, Xiaowei Xu, Hongyong Su, Fengbiao Guo and 6 more

Abstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Article
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  8. iMetaOmics · 2025
    Article
  9. Article
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  11. Article
  12. Study ofInternational journal of inflammation · 2025
    Article
  13. Review
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  15. 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

16 authors.

Jiaxuan Chen *Department of Nephrology, National Clinical Key Specialty Construction Program, Institute of Nephrology, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Laboratory Medicine Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Quanren Pan *Department of Nephrology, National Clinical Key Specialty Construction Program, Institute of Nephrology, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Laboratory Medicine Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Lu Lu *Department of Nephrology, National Clinical Key Specialty Construction Program, Institute of Nephrology, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Laboratory Medicine Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Xiaorong Huang *Department of Nephrology, National Clinical Key Specialty Construction Program, Institute of Nephrology, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Laboratory Medicine Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Shuting WangDepartment of Nephrology, National Clinical Key Specialty Construction Program, Institute of Nephrology, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Laboratory Medicine Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Xiaoxian LiuDepartment of Nephrology, National Clinical Key Specialty Construction Program, Institute of Nephrology, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Laboratory Medicine Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Jiaqi LunDepartment of Nephrology, National Clinical Key Specialty Construction Program, Institute of Nephrology, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Laboratory Medicine Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Xiaowei XuDepartment of Nephrology, National Clinical Key Specialty Construction Program, Institute of Nephrology, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Laboratory Medicine Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Hongyong SuDepartment of Nephrology, National Clinical Key Specialty Construction Program, Institute of Nephrology, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Laboratory Medicine Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Fengbiao GuoDepartment of Nephrology, National Clinical Key Specialty Construction Program, Institute of Nephrology, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Laboratory Medicine Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Lawei YangDepartment of Nephrology, National Clinical Key Specialty Construction Program, Institute of Nephrology, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Laboratory Medicine Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Liuyong YouDepartment of Clinical Laboratory, State Key Laboratory of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Haiyan XiaoDepartment of Cellular Biology and Anatomy, James and Jean Culver Vision Discovery Institute, Medical College of Georgia, Augusta University, Augusta, GA, USA.
Wenying LuoDepartment of Nephrology, National Clinical Key Specialty Construction Program, Institute of Nephrology, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Laboratory Medicine Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Hua-Feng LiuDepartment of Nephrology, National Clinical Key Specialty Construction Program, Institute of Nephrology, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Laboratory Medicine Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China. liuhf@gdmu.edu.cn.
Qingjun PanDepartment of Nephrology, National Clinical Key Specialty Construction Program, Institute of Nephrology, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Laboratory Medicine Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China. pqj@gdmu.edu.cn.

Funding

Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Noncommunicable Diseases 2022B1212030003National Natural Science Foundation of China No. 82070757, 82270770Science and Technology Planning Project of Zhanjiang City 2021A05067
6 · The paper itself

Abstract

Autophagic activation in immune cells, gut microbiota dysbiosis, and metabolic abnormalities have been reported separately as characteristics of systemic lupus erythematosus (SLE). Elucidating the crosstalk among the immune system, commensal microbiota, and metabolites is crucial to understanding the pathogenesis of autoimmune diseases. Emerging evidence shows that basophil activation plays a critical role in the pathogenesis of SLE; however, the underlying mechanisms remain largely unknown. Here, we investigated the effects of autophagic inhibition on the pathogenesis of basophils in SLE using Autophagy-related gene 5 (Atg5) knockout (Atg5

Indexed as

Autophagy-Related Protein 5BasophilsDysbiosisGastrointestinal MicrobiomeLupus Erythematosus, SystemicAnimalsAutophagyFemaleMiceMice, Inbred MRL lprMice, KnockoutAtg5 protein, mouseAutophagy-Related Protein 5Atg5AutoantibodiesBasophilsGut microbiotaInflammatory cytokinesLupusMetabolism

Identifiers

PMID39844180
PMCPMC11756211

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Registered trials

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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.