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Upregulation of TLR2 in keratinocytes activates the MAPK pathway and plays a role in the pathogenesis of hidradenitis suppurativa.
J Dermatol Sci
November 2024
Department of Dermatology, Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. Electronic address:
Background: Mutations in gamma-secretase complex (GSC) genes are associated with hidradenitis suppurativa (HS), and toll-like receptor (TLR) 2 is elevated in HS lesions. However, it remains unclear whether TLR2 is upregulated in the skin lesions of patients with HS with GSC gene variants, and the role of its upregulation in the pathogenesis of this disease are unknown.
Objective: To investigate the role of TLR2 upregulation in NCSTN and PSENEN knockdown keratinocytes.
Bioinformatics based exploration of the anti-NAFLD mechanism of Wang's empirical formula via TLR4/NF-κB/COX2 pathway.
Mol Med
December 2024
Disease Prevention and Health Management Center, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310006, Zhejiang, China.
Background: Nonalcoholic fatty liver disease (NAFLD) has developed as a leading public wellness challenge as a result of changes in dietary patterns. Unfortunately, there is still a lack of effective pharmacotherapy methods for NAFLD. Wang's empirical formula (WSF) has demonstrated considerable clinical efficacy in treating metabolic disorders for years.
View Article and Find Full Text PDFEffect of Mechanical Force Stress on the Inflammatory Response in Human Periodontal Ligament Cells.
Int Dent J
December 2024
Center of Excellence for Dental Stem Cell Biology, Faculty of Dentistry, Chulalongkorn University, Bangkok, Thailand; Faculty of Dentistry, Department of Anatomy, Chulalongkorn University, Bangkok, Thailand.
Human periodontal ligament (hPDL) is continuously exposed to mechanical forces that can induce inflammatory responses in resident stem cells (hPDLSCs). Here, we review the impact of mechanical force on hPDLSCs, focusing on the activation of inflammatory cytokines and related signalling pathways, which subsequently influence periodontal tissue remodelling. The effects of various mechanical forces, including compressive, shear, and tensile forces, on hPDLSCs are discussed.
View Article and Find Full Text PDFProtein shapeshifting in necroptotic cell death signaling.
Trends Biochem Sci
December 2024
Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, VIC 3052, Australia; Department of Medical Biology, University of Melbourne, Parkville, VIC 3052, Australia; Drug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC 3052, Australia. Electronic address:
Necroptosis is a mode of programmed cell death executed by the mixed lineage kinase domain-like (MLKL) pseudokinase following its activation by the upstream receptor-interacting protein kinase-3 (RIPK3), subsequent to activation of death, Toll-like, and pathogen receptors. The pathway originates in innate immunity, although interest has surged in therapeutically targeting necroptosis owing to its dysregulation in inflammatory diseases. Here, we explore how protein conformation and higher order assembly of the pathway effectors - Z-DNA-binding protein-1 (ZBP1), RIPK1, RIPK3, and MLKL - can be modulated by post-translational modifications, such as phosphorylation, ubiquitylation, and lipidation, and intermolecular interactions to tune activities and modulate necroptotic signaling flux.
View Article and Find Full Text PDFRole of Toll-like receptor 2 during infection of Leptospira spp: A systematic review.
PLoS One
December 2024
International Vaccine Institute, Seoul, Republic of Korea.
The involvement of Toll-like receptor 2 (TLR2) in leptospirosis is poorly understood. Our systematic review examined its role across in-vitro, in-vivo, ex-vivo, and human studies. Original articles published in English up to January 2024, exploring the role of TLR2 during leptospirosis, were selected from databases including PubMed, Web of Science, Scopus, Trip, and Google Scholar.
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