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In vitro studies have shown that the combination of plasminogen and uPA, but not either protein alone, activated C3 and C5 to the anaphylatoxins C3a and C5a, respectively, and this effect was inhibited by amiloride, an off-target inhibitor of uPA ( Proteinuria-induced tubular cell apoptosis and tubular injury Evidence from several in vitro and in vivo studies suggests that proteinuria causes tubular cell apoptosis, which is involved in the pathogenesis of tubular atrophy ( Proximal tubular cell apoptosis was reported to contribute to glomerular-tubule disconnection with the eventual formation of atubular glomeruli in several congenital and acquired kidney diseases, more frequently in tubulointerstitial disorders, including pyelonephritis and obstructive nephropathy, but also in disorders of glomerular origin, such as chronic glomerulonephritis and diabetic nephropathy ( Accumulating evidence indicates that during albumin overload, aberrantly filtered free fatty acids (also known as non-esterified fatty acids) bound to albumin are reabsorbed by the proximal tubule and contribute to cytotoxicity ( Slc27a2 ) resulted in the mitigation of proximal tubular cell apoptosis and tubular atrophy compared to wild-type animals with albuminuria ( Slc27a2 in two mouse models of diabetic kidney disease led to attenuation of tubular atrophy, albuminuria and glomerular filtration rate decline compared with diabetic mice expressing FATP2 ( Slc27a2 knockout mice also exhibited remarkably reduced fasting glycemia, which could have conferred indirect kidney benefits ( Involvement of endoplasmic reticulum stress in proteinuria-induced tubular cell apoptosis and tubular injury Proteinuria can trigger tubular cell apoptosis also by inducing endoplasmic reticulum (ER) stress, a change in ER homeostasis due to the accumulation of unfolded or misfolded proteins, which leads to the activation of the unfolded protein response (UPR)
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LeRoith D, Roberts CT Jr
