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http://dx.doi.org/10.1007/978-1-4899-5037-6_20 | DOI Listing |
J Pharm Bioallied Sci
April 2024
Department of Clinical Sciences, College of Dentistry, Centre of Medical and Bio-Allied Health Sciences and Research, Ajman University, Ajman, UAE.
Matrix metalloproteinase-1 (MMP-1) plays a pivotal role in the pathogenesis of periodontal diseases, particularly periodontitis, by virtue of its collagenolytic activity targeting collagen type I, the primary component of periodontal tissues. This review abstract elucidates the intricate involvement of MMP-1 in periodontal tissue homeostasis and its dysregulation in disease states. Elevated MMP-1 levels, observed in gingival tissues and crevicular fluid of individuals with periodontitis, correlate with the degradation of collagen fibers within the periodontium.
View Article and Find Full Text PDFEur Respir Rev
April 2024
School of Pharmacy, Queen's University Belfast, Belfast, UK
Proc Natl Acad Sci U S A
February 2024
Department of Physiology/Metabolic Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Gothenburg 405 30, Sweden.
Efficient removal of fibrillar collagen is essential for adaptive subcutaneous adipose tissue (SAT) expansion that protects against ectopic lipid deposition during weight gain. Here, we used mice to further define the mechanism for this collagenolytic process. We show that loss of collagen type-1 (CT1) and increased CT1-fragment levels in expanding SAT are associated with proliferation of resident M2-like macrophages that display increased CD206-mediated engagement in collagen endocytosis compared to chow-fed controls.
View Article and Find Full Text PDFAdv Sci (Weinh)
April 2024
Department of Pathology and Pathophysiology, and Department of Respiratory Medicine at Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310058, China.
Curr Mol Pharmacol
November 2023
Division of Rheumatology, Allergy, and Immunology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan.
Background: Rheumatoid arthritis (RA) is a systemic inflammatory disease in which TNF-α plays an important role. Fibroblast growth factor receptor 3 (FGFR3) is reportedly involved in RA by regulating the expression of inflammatory cytokines.
Objective: This study examined the expression profile of FGFR3 in human synovial biopsy tissues and evaluated its gene-silencing effects on behaviors of synovial cells.
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