Evidence map›Paper›PMID 40641872›Full record

ReviewFrontiers in microbiology2025

Host SUMOylation in bacterial infections and immune defense mechanisms.

Yuhua Xu, Xi Ma, Zhifeng Wu, Ruitong Huang, Chenhua Liao, Di Huang, Yujun Tang, Chengbin Zhu, Yaqi Wang, Siyuan Zhang and 2 more

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. 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

12 authors.

Yuhua XuInstitute of Pathogenic Biology, Basic Medical School, Hengyang Medical School, Hengyang Central Hospital, University of South China, Hengyang, Hunan, China.
Xi MaInstitute of Pathogenic Biology, Basic Medical School, Hengyang Medical School, Hengyang Central Hospital, University of South China, Hengyang, Hunan, China.
Zhifeng WuInstitute of Pathogenic Biology, Basic Medical School, Hengyang Medical School, Hengyang Central Hospital, University of South China, Hengyang, Hunan, China.
Ruitong HuangInstitute of Pathogenic Biology, Basic Medical School, Hengyang Medical School, Hengyang Central Hospital, University of South China, Hengyang, Hunan, China.
Chenhua LiaoInstitute of Pathogenic Biology, Basic Medical School, Hengyang Medical School, Hengyang Central Hospital, University of South China, Hengyang, Hunan, China.
Di HuangInstitute of Pathogenic Biology, Basic Medical School, Hengyang Medical School, Hengyang Central Hospital, University of South China, Hengyang, Hunan, China.
Yujun TangPlastic Surgery Department, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Chengbin ZhuHengyang Chinese Medicine Hospital, Hengyang, Hunan, China.
Yaqi WangInstitute of Pathogenic Biology, Basic Medical School, Hengyang Medical School, Hengyang Central Hospital, University of South China, Hengyang, Hunan, China.
Siyuan ZhangInstitute of Pathogenic Biology, Basic Medical School, Hengyang Medical School, Hengyang Central Hospital, University of South China, Hengyang, Hunan, China.
Peng LiuInstitute of Pathogenic Biology, Basic Medical School, Hengyang Medical School, Hengyang Central Hospital, University of South China, Hengyang, Hunan, China.
Jiaofeng PengInstitute of Pathogenic Biology, Basic Medical School, Hengyang Medical School, Hengyang Central Hospital, University of South China, Hengyang, Hunan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SUMOylation, the covalent attachment of small ubiquitin-like modifier proteins (SUMO) to lysine residues of target substrates, has emerged as a crucial post-translational modification regulating various cellular processes. Recent studies have revealed that SUMOylation also plays significant roles in host-pathogen interactions during bacterial infections. On the one hand, SUMOylation can modulate host innate immune responses, such as inflammatory signaling and autophagy, to defend against invading bacteria. On the other hand, certain bacterial pathogens have evolved strategies to exploit or manipulate the host SUMOylation machinery to promote their survival and replication. Some bacterial effector proteins directly target host SUMO enzymes or SUMO-conjugated substrates to disrupt host defense mechanisms. This review summarizes the current understanding of the complex interplay between SUMOylation and bacterial infection, highlighting the dual roles of SUMOylation in host defense and bacterial pathogenesis. We discuss the mechanisms by which SUMOylation regulates host immune responses against bacterial infection and how bacterial pathogens hijack host SUMOylation for their own benefit. Moreover, we explore the potential of targeting SUMOylation as a novel therapeutic strategy for combating bacterial infections. Further research into the intricate relationship between SUMOylation and bacterial infection may provide valuable insights for developing innovative anti-infective therapies.

Indexed as

bacterial infectionbacterial pathogenesishost-pathogen interactioninnate immunitySUMOSUMOylation

Identifiers

PMID40641872
PMCPMC12241045

What OpenQuestion holds

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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.