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Epithelium-derived exosomal dipeptidyl peptidase-4 involved in arecoline-induced oral submucous fibrosis.
Biochim Biophys Acta Mol Basis Dis
January 2025
Department of Healthcare Administration, Asia University, 40454 Taichung, Taiwan. Electronic address:
Introduction: Dipeptidyl peptidase-4 is known to be involved in the progression of several fibrogenic diseases, but its association with oral submucous fibrosis remains unclear. This study aims to ascertain whether dipeptidyl peptidase-4 plays a role in the pathogenesis of arecoline-induced oral submucous fibrosis.
Methods: We assessed the expression of dipeptidyl peptidase-4 in arecoline-treated epithelial cells and the exosomes derived from cells.
Tissue fibrosis in cardiorenal syndrome: crosstalk between heart and kidneys.
Nephrol Dial Transplant
January 2025
School of Biosciences and Bioengineering, Indian Institute of Technology (IIT), Mandi, Himachal Pradesh, India.
Cardiorenal syndrome (CRS) is represented as an intricate dysfunctional interplay between the heart and kidneys, marked by cardiorenal inflammation and fibrosis. Unlike other organs, the repair process in cardiorenal injury involves a regenerative phase characterized by proliferation and polyploidization, followed by a subsequent pathogenic phase of fibrosis. In CRS, acute or chronic cardiorenal injury leads to hyperactive inflammation and fibrotic remodeling, associated with injury-mediated immune cell (Macrophages, Monocytes, and T-cells) infiltration and myofibroblast activation.
View Article and Find Full Text PDFRegulation of fibronectin and collagens type I, III and VI by TNF-α, TGF-β, IL-13, and tofacitinib.
Sci Rep
January 2025
Nordic Bioscience, Immunoscience, Herlev Hovedgade 205-207, Herlev, 2730, Denmark.
Understanding how inflammatory cytokines influence profibrogenic wound healing responses in fibroblasts is important for understanding the pathogenesis of fibrosis. TNF-α and IL-13 are key cytokines in Th1 and Th2 immune responses, respectively, while TGF-β1 is the principal pro-fibrotic mediator. We show that 12-day fibroblast culture with TNF-α or IL-13 induces fibrogenesis, marked by progressively increasing type III and VI collagen formation, and that TGF-β1 co-stimulation amplifies these effects.
View Article and Find Full Text PDFMindin/spondin-2 regulates fibroblast subpopulations through distinct Src family kinases during fibrogenesis.
JCI Insight
December 2024
Center for Inflammation and Tissue Homeostasis, Institute for Stem Cell Science and Regenerative Medicine, Bangalore, India.
Fibrosis results from excessive extracellular matrix (ECM) deposition, causing tissue stiffening and organ dysfunction. Activated fibroblasts, central to fibrosis, exhibit increased migration, proliferation, contraction, and ECM production. However, it remains unclear if the same fibroblast performs all of the processes that fall under the umbrella term of "activation".
View Article and Find Full Text PDFDextromethorphan inhibits collagen and collagen-like cargo secretion to ameliorate lung fibrosis.
Sci Transl Med
December 2024
Cell Biology and Biophysics Unit, European Molecular Biology Laboratory, 69117 Heidelberg, Germany.
Excessive deposition of fibrillar collagen in the interstitial extracellular matrix (ECM) of human lung tissue causes fibrosis, which can ultimately lead to organ failure. Despite our understanding of the molecular mechanisms underlying the disease, no cure for pulmonary fibrosis has yet been found. We screened a drug library and found that dextromethorphan (DXM), a cough expectorant, reduced the amount of excess fibrillar collagen deposited in the ECM in cultured primary human lung fibroblasts, a bleomycin mouse model, and a cultured human precision-cut lung slice model of lung fibrosis.
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