ArticleAging2019
p38MAPK/SGK1 signaling regulates macrophage polarization in experimental autoimmune encephalomyelitis.
Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- The Mechanistic Review of the Molecular Interface of RNA-Loaded Extracellular Vesicles: Redefining Targeted Therapy for Autoimmune Disorders.International journal of molecular sciences · 2026Review
- Medicinal Plants Facilitate the Recovery of Diabetic Foot Ulcer by Regulating Macrophages: Latest Evidence and Insights.Current diabetes reviews · 2026Review
- Graphene oxide-engineered dental implants: orchestrating antibacterial defense and osteo-immunomodulation for enhanced osseointegration.Frontiers in bioengineering and biotechnology · 2026Article
- Immune cell involvement in ulcer repair in radiation esophagitis and its role in the TGF-β1/p38MAPK/FN axis (Review).Molecular and clinical oncology · 2025Review
- Immune micro-environment analysis and drug screening for ovarian endometriosis.Genes & genomics · 2024Article
- SFRP1 decreases WNT-Mediated M2 macrophage marker expression in breast tissue.Cancer immunology, immunotherapy : CII · 2024Article
- Immunomodulatory effects of curcumin on macrophage polarization in rheumatoid arthritis.Frontiers in pharmacology · 2024Review
- Role of Serum/Glucocorticoid-Regulated Kinase 1 (SGK1) in Immune and Inflammatory Diseases.Inflammation · 2023Review
- Regulatory Mechanism of M1/M2 Macrophage Polarization in the Development of Autoimmune Diseases.Mediators of inflammation · 2023Review
- Serum- and Glucocorticoid-Inducible Kinase 1 Promotes Alternative Macrophage Polarization and Restrains Inflammation through FoxO1 and STAT3 Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- M-CSF, IL-6, and TGF-β promote generation of a new subset of tissue repair macrophage for traumatic brain injury recovery.Science advances · 2021Article
- Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is characterized with multifocal demyelination resulting from activation and infiltration of inflammatory cells into the central nerve system. Recent reports suggest that p38 mitogen-activated protein kinase (MAPK) / serum- and glucocorticoid-inducible protein kinase 1 (SGK1) signaling pathway contributes to the pathology of MS through regulation of immunity. However, the role of this signaling pathway in MS-related macrophage activation and polarization has not been studied. Here, we used an experimental autoimmune encephalomyelitis (EAE) model for MS to study the role of p38MAPK/SGK1 signaling in the macrophage polarization and its effects on the development and severity of EAE. Here, we found that p38MAPK/SGK1 signaling is required for IL4-induced M2 macrophage polarization in vitro. Chitin-induced M2 macrophage polarization reduces the severity of EAE in mice. Generation of an adeno-associated virus (AAV) carrying sh-p38 or sh-SGK1 under the control of a CD68 promoter successfully knockdown p38 or SGK1 levels in vitro and in vivo. Treatment with AAV-sh-p38 or AAV-sh-SGK1 abolished the effects of Chitin on macrophage polarization and the severity of EAE. Thus, our data suggest that p38MAPK/SGK1 signaling induces M2 macrophage polarization, which reduces the severity of EAE, a model for MS.
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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.