Evidence map›Paper›PMID 39806430›Full record

ReviewCell communication and signaling : CCS2025

Histone demethylases in autophagy and inflammation.

Yaoyao Ma, Wenting Lv, Yi Guo, Tong Yin, Yujie Bai, Ziqi Liu, Chao Chen, WenjuanYang, Jiayi Feng, Wenbin Qian and 6 more

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. Autophagy in the liver.Autophagy reports · 2026
    Review
  3. Review
  4. Article
  5. Article
  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

16 authors.

Yaoyao Ma *Hubei Key Laboratory of Diabetes and Angiopathy, School of Pharmacy, Hubei University of Science and Technology, Hubei, 437000, China.
Wenting Lv *3Hubei Province Key Laboratory of Allergy and Immunology, School of Basic Medical Sciences, Wuhan University, Hubei, 430071, China.
Yi Guo *School of Basic Medical Sciences, Hubei University of Science and Technology, Hubei, 437000, China.
Tong Yin *3Hubei Province Key Laboratory of Allergy and Immunology, School of Basic Medical Sciences, Wuhan University, Hubei, 430071, China.
Yujie BaiDepartment of Scientific Research and Education, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, 330000, China.
Ziqi Liu3Hubei Province Key Laboratory of Allergy and Immunology, School of Basic Medical Sciences, Wuhan University, Hubei, 430071, China.
Chao ChenSchool of Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
WenjuanYang3Hubei Province Key Laboratory of Allergy and Immunology, School of Basic Medical Sciences, Wuhan University, Hubei, 430071, China.
Jiayi Feng3Hubei Province Key Laboratory of Allergy and Immunology, School of Basic Medical Sciences, Wuhan University, Hubei, 430071, China.
Wenbin QianHubei Key Laboratory of Diabetes and Angiopathy, School of Pharmacy, Hubei University of Science and Technology, Hubei, 437000, China.
Ruiling TangHubei Key Laboratory of Diabetes and Angiopathy, School of Pharmacy, Hubei University of Science and Technology, Hubei, 437000, China.
Yanting SuHubei Key Laboratory of Diabetes and Angiopathy, School of Pharmacy, Hubei University of Science and Technology, Hubei, 437000, China.
Shigang ShanSchool of Public Health and Nursing, Hubei University of Science and Technology, Hubei, 437000, China.
Huifen Dong3Hubei Province Key Laboratory of Allergy and Immunology, School of Basic Medical Sciences, Wuhan University, Hubei, 430071, China. hfdong@whu.edu.cn.
Yongfen BaoSchool of Basic Medical Sciences, Hubei University of Science and Technology, Hubei, 437000, China. 45854259@qq.com.
Lihua QuSchool of Basic Medical Sciences, Hubei University of Science and Technology, Hubei, 437000, China. lihuaqu@whu.edu.cn.

Funding

Hubei University of Science and Technology Development Fund Project BK202442Innovation Team of Hubei University of Science and Technology 2023T13National Natural Science Foundation of China 82172301Natural Science Foundation of Hubei Province, China JCZRQN202401149
6 · The paper itself

Abstract

Autophagy dysfunction is associated with changes in autophagy-related genes. Various factors are connected to autophagy, and the mechanism regulating autophagy is highly complicated. Epigenetic changes, such as aberrant expression of histone demethylase, are actively associated not only with oncogenesis but also with inflammatory responses. Among post-translational modifications, histone lysine methylation holds significant importance. There are over 30 members of histone lysine demethylases (KDMs), which act as epigenetic regulators in physiological processes and diseases. Importantly, KDMs are abnormally expressed in the regulation of cellular autophagy and inflammation, representing a crucial mechanism affecting inflammation-related diseases. This article reviewed the function of KDMs proteins in autophagy and inflammation. Specifically, It focused on the specific regulatory mechanisms underlying the activation or inhibition of autophagy, as well as their abnormal expression in inflammatory responses. By analyzing each KDM in epigenetic modification, this review provides a reliable theoretical basis for clinical decision marking regarding autophagy abnormalities and inflammatory diseases.

Indexed as

AutophagyHistone DemethylasesInflammationAnimalsEpigenesis, GeneticHumansHistone DemethylasesAutophagyHistone demethylasesInflammation

Identifiers

PMID39806430
PMCPMC11727796

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.