Morphometric Effects of HO-1 Deficiency and Overexpression in Rat Glomeruli and Podocytes

Of the various cells comprising the glomerulus (endothelial, mesangial, resident macrophages, and visceral glomerular epithelial cells also known as podocytes), the latter are most vulnerable to various forms of glomerular injury (Diabetes, Hypertension, immunemediated, etc.) that frequently progress to end-stage kidney disease (ESKD). This is due to their non-replicative, terminally differentiated highly specialized nature. Specifically, they exhibit a high rate of vesicular traffic as evidenced by multiple coated vesicles and coated pits along their basolateral domain and have a high capacity for protein synthesis and posttranslational modifications because of a well-developed endoplasmic reticulum and a large Golgi apparatus [1]. Podocyte depletion consequent to injury is a well-established mechanism underlying glomerular scarring (sclerosis) while progressive glomerulosclerosis leads to ESKD [2]. It is, therefore, not surprising that strategies assessing ways to protect podocytes against injury are being explored.