TRPC5 and glomerular disorder: TRPC5, a novel target in podocyte disorders,[10] when inhibited, stimulates the regeneration of the podocyte foot process and restores kidney filter function.[22] However, no previous research has identified a potential candidate targeting Ca2+ signaling in podocytes via TRPC5, influencing mitochondrial respiration and cell viability.[6] In the ADN mouse model, GQDs enhanced podocyte function and mitochondrial efficiency, offering a novel approach to addressing glomerular disorders.