Evidence map›Paper›PMID 40662732›Full record

ArticlemBio2025

Interferon-stimulated circHOMER1 attenuates antiviral innate immunity.

Ao Zhang, Ranran Yao, Shijin Geng, Haiying Wang, Rong-Chun Tang, Hengxiang Yu, Rui Xu, Hong-Yan Chen, Yunxuan Zhou, Lan Zhang and 1 more

Abstract read
In one paragraph

Article in mBio, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Circular RNAScience advances · 2026
    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

11 authors.

Ao Zhang *Department of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Medicine Innovation Center for Fundamental Research on Major Immunology-related Diseases, Peking University, Beijing, China.ORCID 0009-0003-6778-7901
Ranran Yao *Department of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Medicine Innovation Center for Fundamental Research on Major Immunology-related Diseases, Peking University, Beijing, China.
Shijin GengDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Medicine Innovation Center for Fundamental Research on Major Immunology-related Diseases, Peking University, Beijing, China.
Haiying WangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Peking University, Beijing, China.
Rong-Chun TangDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Medicine Innovation Center for Fundamental Research on Major Immunology-related Diseases, Peking University, Beijing, China.
Hengxiang YuDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Medicine Innovation Center for Fundamental Research on Major Immunology-related Diseases, Peking University, Beijing, China.
Rui XuDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Medicine Innovation Center for Fundamental Research on Major Immunology-related Diseases, Peking University, Beijing, China.
Hong-Yan ChenDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Medicine Innovation Center for Fundamental Research on Major Immunology-related Diseases, Peking University, Beijing, China.
Yunxuan ZhouDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Medicine Innovation Center for Fundamental Research on Major Immunology-related Diseases, Peking University, Beijing, China.
Lan ZhangDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Medicine Innovation Center for Fundamental Research on Major Immunology-related Diseases, Peking University, Beijing, China.
Jun ZhangDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Medicine Innovation Center for Fundamental Research on Major Immunology-related Diseases, Peking University, Beijing, China.ORCID 0000-0001-5147-6963

Funding

Beijing Municipal Natural Science Foundation M23006National Natural Science Foundation of China 82071786,82271796
6 · The paper itself

Abstract

In an initial screening of virus-induced differentially expressed circRNAs, circHOMER1 was significantly upregulated. However, its role in antiviral innate immunity remained unclear. circHOMER1 was upregulated in response to a range of stimuli, including RNA viruses, DNA viruses, as well as type I IFNs. Overexpression of circHOMER1 reduced the virus-induced type I IFN signaling pathway and promoted viral replication. Consistently, knockdown of circHOMER1 yielded opposite consequence. Mechanistically, circHOMER1 acted as a competitive endogenous RNA (ceRNA) for miR-145-3p, controlling the mRNA level of OTU domain-containing protein 7B (OTUD7B), thereby downregulating interferon regulatory factor 3 (IRF3) expression. Furthermore, circHOMER1 was found to disrupt the interaction between Ras GTPase-activating protein-binding protein 1 (G3BP1) and retinoic-acid-inducible protein I (RIG-I), impairing the detection of viral RNAs by RIG-I. Notably, the concordant immunosuppressive effects of circHOMER1 were observed in mouse infection models. These findings identify circHOMER1 as a novel interferon-stimulated circRNA that serves as a negative modulator of the antiviral innate immune response and is essential for immune homeostasis. IMPORTANCE: A growing body of evidence suggests that circRNAs are involved in various physiological or pathological processes. Through circRNA microarray screening of virus-induced differentially expressed circRNAs, we identified an upregulated circRNA, circHOMER1. circHOMER1 is abundantly expressed in the brain. The known functions of circHOMER1 have been focused on the nervous systems and the related diseases. Its functions in the immune system are not discovered. In this study, we found that circHOMER1 is upregulated by viral infection, interferon treatment, etc. circHOMER1 can negatively modulate virus-induced type I IFN signaling by acting as a ceRNA or other mechanism. The regulatory function of circHOMER1 in innate immunity is critical for immune homeostasis. The dysregulation of circHOMER1 may be associated with virus encephalitis or other related diseases. circHOMER1 may be a potential therapeutic target of virus-induced infections and autoimmune diseases.

Indexed as

Immunity, InnateInterferonsInterferon Type IRNA, CircularAnimalsDEAD Box Protein 58HumansInterferon Regulatory Factor-3MiceMice, Inbred C57BLMicroRNAsSignal TransductionVirus DiseasesVirus ReplicationDEAD Box Protein 58Interferon Regulatory Factor-3InterferonsInterferon Type IMicroRNAsRNA, CircularceRNAcircHOMER1innate immunitymiR-145-3pRIG-I

Identifiers

PMID40662732
PMCPMC12345189

What OpenQuestion holds

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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.