Evidence map›Paper›PMID 41220006›Full record

ReviewCell communication and signaling : CCS2025

Protein acylation in inflammatory diseases: from mechanisms to therapeutic strategies.

Jiayi Ding, Huiyi Wang, Zhengkun Yang, Xiaoxuan Wang, Zhengguo Cao

Abstract readReview
In one paragraph

Review 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 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. Article
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  6. 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

5 authors.

Jiayi Ding *State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Huiyi Wang *State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Zhengkun YangState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Xiaoxuan WangState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China. wangxiaoxuan@whu.edu.cn.
Zhengguo CaoState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China. caozhengguo@whu.edu.cn.

Funding

National Key Research and Development Program of China 2023YFC2506300National Natural Science Foundation of China 82101022National Natural Science Foundation of China 82170963, 82370967
6 · The paper itself

Abstract

Protein acylation, a critical subset of post-translational modifications (PTMs), serves as a dynamic regulatory mechanism linking cellular metabolism, epigenetic regulation, and inflammatory responses. This review systematically elucidates the roles of protein acylation modifications-including acetylation, lactylation, succinylation, propionylation, crotonylation, malonylation, butyrylation, S-palmitoylation, and myristoylation-in the pathogenesis of inflammatory diseases. These modifications, orchestrated by acyltransferases (writers), deacylases (erasers), and recognition proteins (readers), regulate immune cell functionality and disease progression. In immune cells, specific acylation patterns govern inflammatory responses by modulating polarization, cytokine production, and signaling pathways. Furthermore, dysregulated protein acylation contributes to the pathogenesis of inflammatory diseases such as sepsis, periodontitis, inflammatory bowel disease, atherosclerosis, and rheumatoid arthritis through disrupting immune homeostasis, driving metabolic reprogramming, and impairing tissue repair. Emerging therapeutic strategies targeting acylation-related enzymes or leveraging nanoparticle-based drug delivery systems show promise in restoring balanced PTM dynamics and alleviating disease progression. By systematically mapping protein acylation networks across immune and diseased cells, this review provides insights into novel diagnostic biomarkers and therapeutic interventions for inflammatory diseases.

Indexed as

InflammationProtein Processing, Post-TranslationalProteinsAcylationAnimalsHumansProteinsInflammatory diseasesPost-translational modificationsProtein acylation

Identifiers

PMID41220006
PMCPMC12607008

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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.