Key PointsGenetically induced decay-accelerating factor (DAF) overexpression prevents adriamycin (ADR)-induced focal segmental glomerulosclerosis (FSGS) in mice.Pharmacologic inhibition of DAF cleavage reduces complement activation in the glomeruli and albuminuria in murine ADR-induced FSGS.Inhibition of complement activation represents a valuable therapeutic strategy for FSGS and, potentially, other glomerular diseases.
Bin, S., Budge, K., Gentile, M., Podesta, M.A., Khan, Y., Azzi, J.R., et al. (2023). Decay-Accelerating Factor Expression Modulates the Severity of Experimental Focal Segmental Glomerulosclerosis. KIDNEY360, 4(3), 381-386 [10.34067/KID.0005312022].
Decay-Accelerating Factor Expression Modulates the Severity of Experimental Focal Segmental Glomerulosclerosis
Bin S.Primo
;Khan Y.;La Manna G.;
2023
Abstract
Key PointsGenetically induced decay-accelerating factor (DAF) overexpression prevents adriamycin (ADR)-induced focal segmental glomerulosclerosis (FSGS) in mice.Pharmacologic inhibition of DAF cleavage reduces complement activation in the glomeruli and albuminuria in murine ADR-induced FSGS.Inhibition of complement activation represents a valuable therapeutic strategy for FSGS and, potentially, other glomerular diseases.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
