NIH R01 · 2024
PROJECT SUMMARY Canonical transient receptor potential-6 (TRPC6) channels drive certain familial forms of focal and segmental glomerulosclerosis (FSGS) and there is evidence that they contribute to much more common acquired forms of FSGS and to renal fibrosis. TRPC6 dysregulation in podocytes occurs in animal models of FSGS, and in podocytes exposed to serum or plasma from patients with recurrent FSGS, or in cells treated with the soluble urokinase receptor (suPAR). While it is known that TRPC6 activation is required for Ca2+ influx driven by e.g. angiotensin II, the Ca2+-permeability of TRPC6 is quite limited, and there are many conditions in which TRPC6 functions primarily as a monovalent…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.