Evidence map›Paper›PMID 39537902›Full record

ArticleCellular & molecular immunology2024

Alternative mRNA polyadenylation regulates macrophage hyperactivation via the autophagy pathway.

Yunzhu Chen, Baiwen Chen, Jingyu Li, Haixin Li, Gaoyang Wang, Xuemin Cai, Qianqian Zhang, Xiaoxu Liu, Chen Kan, Lei Wang and 2 more

Abstract read
In one paragraph

Article in Cellular & molecular immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

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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.

Yunzhu ChenShanghai Institute of Immunology, State Key Laboratory of Oncogenes and Related Genes, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Baiwen ChenShanghai Institute of Immunology, State Key Laboratory of Oncogenes and Related Genes, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jingyu LiShanghai Institute of Immunology, State Key Laboratory of Oncogenes and Related Genes, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0003-3123-6668
Haixin LiShanghai Institute of Immunology, State Key Laboratory of Oncogenes and Related Genes, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Gaoyang WangShanghai Institute of Immunology, State Key Laboratory of Oncogenes and Related Genes, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xuemin CaiInstitute of Immunological Innovation & Translation, Chongqing Medical University, Chongqing, China.
Qianqian ZhangShanghai Institute of Immunology, State Key Laboratory of Oncogenes and Related Genes, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiaoxu LiuShanghai Institute of Immunology, State Key Laboratory of Oncogenes and Related Genes, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Chen KanSchool of Biological Science, The University of Manchester, Manchester, UK.
Lei WangDepartment of Geriatrics, Medical Center on Aging of Shanghai Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Zhengting WangDepartment of Gastroenterology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Hua-Bing LiShanghai Institute of Immunology, State Key Laboratory of Oncogenes and Related Genes, Shanghai Jiao Tong University School of Medicine, Shanghai, China. huabing.li@shsmu.edu.cn.ORCID 0000-0003-3573-6803

Funding

Ministry of Science and Technology of the People's Republic of China (Chinese Ministry of Science and Technology) 2021YFA1100800National Natural Science Foundation of China (National Science Foundation of China) 32070917National Natural Science Foundation of China (National Science Foundation of China) 82030042National Natural Science Foundation of China (National Science Foundation of China) 82325024National Natural Science Foundation of China (National Science Foundation of China) 82350112
6 · The paper itself

Abstract

Macrophage hyperactivation is a hallmark of inflammatory diseases, yet the role of alternative polyadenylation (APA) of mRNAs in regulating innate immunity remains unclear. In this study, we focused on 3'UTR-APA and demonstrated that Nudt21, a crucial RNA-binding component of the 3'UTR-APA machinery, is significantly upregulated in various inflammatory conditions. By utilizing myeloid-specific Nudt21-deficient mice, we revealed a protective effect of Nudt21 depletion against colitis and severe hyperinflammation, primarily through diminished production of proinflammatory cytokines. Notably, Nudt21 regulates the mRNA stability of key autophagy-related genes, Map1lc3b and Ulk2, by mediating selective 3'UTR polyadenylation in activated macrophages. As a result, Nudt21-deficient macrophages display increased autophagic activity, which leads to reduced cytokine secretion. Our findings highlight an unexplored role of Nudt21-mediated 3'UTR-APA in modulating macrophage autophagy and offer new insights into the modulation of inflammation and disease progression.

Indexed as

3' Untranslated RegionsAutophagyMacrophage ActivationMacrophagesPolyadenylationRNA, MessengerAnimalsColitisCytokinesHumansInflammationMiceMice, Inbred C57BLMice, KnockoutRNA Stability3' Untranslated RegionsCytokinesRNA, Messengeralternative polyadenylationautophagyinflammationmacrophageNudt21

Identifiers

PMID39537902
PMCPMC11607066

What Socratic 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 Socratic graph.