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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Animals, Base Sequence, Collagen Type I, DNA Primers, Fibroblasts, Fibrosis, Kidney Diseases, Macrophages, Male, Mice, Mice, Inbred C57BL, Phosphorylation, Protein Kinase Inhibitors, Pyrazoles, Pyridines, RNA, Messenger, Time Factors, Transforming Growth Factor beta1, Ureteral Obstruction, p38 Mitogen-Activated Protein Kinases.
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Does delayed inhibition of p38 mitogen-activated protein kinase ameliorate renal fibrosis in obstructive nephropathy? Context: The p38 mitogen-activated protein kinase (MAPK) pathway is an important intracellular signalling pathway involved in the production of proinflammatory and profibrotic mediators. Previous reports indicated the role of p38 MAPK activation in renal fibrosis. We administered a selective p38 alpha MAPK inhibitor, FR167653, in a mouse model of unilateral ureteral obstruction (UUO) during the late stage (Days 7-14) after UUO, and the kidneys were examined at Day 14. p38 and phospho-p38 MAPK protein levels, the degree of renal fibrosis, the degree of myofibroblast accumulation and macrophage infiltration, and mRNA levels for TGF-beta1 and alpha1(I) collagen in the kidneys were assessed. FR167653 treatment caused marked decreases in phospho-p38 MAPK levels along with decreased fibrosis at Day 14 after UUO. Although myofibroblast accumulation and alpha1(I) collagen mRNA level were decreased, no significant change was observed in the number of interstitial macrophages and TGF-beta1 mRNA level with FR167653 treatment.
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These results suggest that p38 MAPK blockade is an appealing therapeutic target, even after the emergence of established fibrosis. Final Decision: yes