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Review
. 2017:982:563-575.
doi: 10.1007/978-3-319-55330-6_29.

Prohibitin Signaling at the Kidney Filtration Barrier

Christina Ising  1   2 , Paul T Brinkkoetter  3
Affiliations
Review

Prohibitin Signaling at the Kidney Filtration Barrier

Christina Ising et al. Adv Exp Med Biol. 2017.

Abstract

The kidney filtration barrier consists of three well-defined anatomic layers comprising a fenestrated endothelium, the glomerular basement membrane (GBM) and glomerular epithelial cells, the podocytes. Podocytes are post-mitotic and terminally differentiated cells with primary and secondary processes. The latter are connected by a unique cell-cell contact, the slit diaphragm. Podocytes maintain the GBM and seal the kidney filtration barrier to prevent the onset of proteinuria. Loss of prohibitin-1/2 (PHB1/2) in podocytes results not only in a disturbed mitochondrial structure but also in an increased insulin/IGF-1 signaling leading to mTOR activation and a detrimental metabolic switch. As a consequence, PHB-knockout podocytes develop proteinuria and glomerulosclerosis and eventually loss of renal function. In addition, experimental evidence suggests that PHB1/2 confer additional, extra-mitochondrial functions in podocytes as they localize to the slit diaphragm and thereby stabilize the unique intercellular contact between podocytes required to maintain an effective filtration barrier.

Keywords: Insulin; Kidney filtration barrier; Podocyte; Slit diaphragm.

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