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CaMK4 drives podocyte injury

Podocyte dysfunction is a hallmark of kidney injury and occurs in both autoimmune and nonautoimmune renal diseases. Calcium signaling underlies podocyte injury; however, the factors that promote calcium signaling in podocytes in response to injury are not fully understood. In this episode, George Tsokos and colleagues demonstrate that Ca2+/calmodulin–dependent kinase 4 (CaMK4) is increased in podocytes from patients with lupus nephritis and focal segmental glomerulosclerosis and in mouse models of lupus and kidney injury. Moreover, administration of a CaMK4 inhibitor prevented nephritis in lupus-prone mice and ameliorated podocyte damage in mice with kidney injury. Together, this study identifies CaMK4 activation as a driver of podocyte dysfunction and suggests CaMK4 inhibition be further explored for treating podocytopathies.