
The study demonstrated that proteinuric kidney injury increased kidney lymphangiogenesis, isolevuglandin-producing dendritic cells, and IFN-γ–producing CD4+ T cells. Sodium accumulation in the kidney interstitium enhanced lymphatic endothelial cell (LEC) interaction with antigen-presenting cells, stimulating isolevuglandin-adduct formation. The ET-3/ETBR axis regulated LEC dynamics and lymphatic vessel pumping.
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