COL4A3 and HIV-associated nephropathy: Although these studies measured isolated glomeruli that were not perfused, they detected physiologically meaningful alterations in glomerular elasticity because they demonstrated a reduced E with actin depolymerization (cytochalasin-D and latrunculin) and inhibition of non-muscle myosin II activity (blebbistatin) as well as in two disease states, Tg26 mice, a model of HIV nephropathy, and Col4a3-/- mice, a model of Alport syndrome [15,16].