ArticleEXCLI journal2019
Suppressed androgen receptor expression promotes M2 macrophage reprogramming through the STAT3/SOCS3 pathway.
Article in EXCLI journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
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.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Reprogramming macrophage metabolism for cardiovascular therapy: From molecular pathways to precision nanomedicine.Materials today. Bio · 2026Review
- Androgens are a Key Factor Affecting Immune Related Diseases.The world journal of men's health · 2026Review
- The Multifaceted Role of Androgen Receptor Signaling in Immunity: Implications for Oncology.Molecular cancer research : MCR · 2026Review
- Review
- The multisystem impact of perimenopausal hormonal fluctuations on chronic disease risk.Frontiers in endocrinology · 2026Review
- AR Deficiency Protects Against Sepsis-Induced Acute Lung Injury by Inhibiting Macrophage M1 Polarization and Inflammatory Cytokine Secretion.Inflammation · 2025Article
- Exosomal miR-106a-5p derived from intermittently hypoxic non-small-cell lung cancer increases tumor malignancy.Physiological reports · 2024Article
- Loss of LXN promotes macrophage M2 polarization and PD-L2 expression contributing cancer immune-escape in mice.Cell death discovery · 2022Article
- S100a9 Protects Male Lupus-Prone NZBWF1 Mice From Disease Development.Frontiers in immunology · 2021Article
- Androgen-Mediated Anti-inflammatory Cellular Processes as Therapeutic Targets in Lupus.Frontiers in immunology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages are important mediators of inflammatory cardiovascular diseases, and various macrophage phenotypes exert opposite effects during inflammation. In our previous study, we proved that suppressed androgen receptor (AR) alleviated inflammation during experimental autoimmune myocarditis (EAM). As anti-inflammatory cells, whether M2 macrophages are involved in this process remains unclear. Here, we showed that anti-inflammatory cytokines and M2 macrophages were elevated when AR was suppressed during EAM. In IL-4 stimulation-induced M2 macrophages, impaired AR with ASC-J9 increased the expression of M2 macrophage-related factors. Moreover, suppressed AR expression resulted in macrophage M2 polarization by reducing SOCS3 production and enhancing STAT3 activation. Taken together, our data suggest that AR plays a critical role in macrophage polarization and suppressed redundant AR expression promotes anti-inflammatory M2 macrophages reprogramming. This study suggests a potential therapeutic agent for inflammatory cardiomyopathy through the use of ASC-J9.
Indexed as
Identifiers
30956636PMC6449667W2924166785What OpenQuestion holds
Registered trials
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.