Evidence map›Paper›PMID 40416964›Full record

ReviewFrontiers in immunology2025

SIRT1: potential target in glucocorticoid-resistant diseases.

Jun Xie, Siyi Che, Jiao Liu, Xiaoru Long

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

4 authors.

Jun XieDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders; Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing Key Laboratory of Child Rare Diseases in Infection and Immunity, Chongqing, China.
Siyi CheDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders; Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing Key Laboratory of Child Rare Diseases in Infection and Immunity, Chongqing, China.
Jiao LiuDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders; Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing Key Laboratory of Child Rare Diseases in Infection and Immunity, Chongqing, China.
Xiaoru LongDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders; Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing Key Laboratory of Child Rare Diseases in Infection and Immunity, Chongqing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucocorticoid resistance is a challenging problem in clinical practice. Increasing glucocorticoid sensitivity and reducing resistance are important in the management of certain diseases. In steroid-resistant airway inflammatory diseases, glucocorticoid receptor (GR) expression is reduced, and impaired GR nuclear translocation is closely related to glucocorticoid resistance. Histone deacetylase SIRT1 regulates steroid hormone receptor activity and interacts with the androgen receptor and GR. In some glucocorticoid-resistant diseases, SIRT1 expression is reduced. Here, we review recent advances in the role of SIRT1 in regulating glucocorticoid signaling. First, we describe the structure, tissue expression, and subcellular localization of SIRT1. We also discuss the molecular mechanisms by which SIRT1 regulates glucocorticoid activity and its association with GR, as well as the mechanisms and roles of SIRT1 in several common glucocorticoid-resistant diseases. SIRT1 may serve as a potential therapeutic target, providing an opportunity for the treatment of glucocorticoid-resistant diseases.

Indexed as

Drug ResistanceGlucocorticoidsSirtuin 1AsthmaGene Expression RegulationHumansInflammationReceptors, AndrogenReceptors, GlucocorticoidT-Lymphocytes, Helper-InducerGlucocorticoidsReceptors, AndrogenReceptors, GlucocorticoidSirtuin 1acetylationglucocorticoid receptorglucocorticoid resistanceSIRT1T cell

Identifiers

PMID40416964
PMCPMC12098067

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.