Metabolism, energetics, and lipid biology in the podocyte - cellular cholesterol-mediated glomerular injury

摘要: Chronic kidney disease (CKD) is associated with a high risk of death. Dyslipidemia commonly observed in patients CKD and accompanied by decrease plasma high-density lipoprotein, an increase triglyceride-rich lipoproteins oxidized lipids. The observation that statins may albuminuria but do not stop the progression indicates pathways other than cholesterol synthesis contribute to accumulation kidneys CKD. Recently, it has become clear increased lipid influx impaired reverse transport can promote glomerulosclerosis, tubulointerstitial damage. Lipid-rafts are cholesterol-rich membrane domains important functions regulating fluidity, protein trafficking, assembly signaling molecules. In podocytes, which specialized cells glomerulus, they spatial organization slit diaphragm (SD) under physiological pathological conditions. discovery podocyte-specific proteins such as podocin bind recruit contributing formation SD underlines importance homeostasis podocytes suggests regulator development proteinuric disease. Cellular due synthesis, influx, or decreased efflux emerging concept podocyte biology. This review will focus on role cellular pathogenesis diseases glomerular diseases.