Chapter title |
Prohibitin Signaling at the Kidney Filtration Barrier
|
---|---|
Chapter number | 29 |
Book title |
Mitochondrial Dynamics in Cardiovascular Medicine
|
Published in |
Advances in experimental medicine and biology, May 2017
|
DOI | 10.1007/978-3-319-55330-6_29 |
Pubmed ID | |
Book ISBNs |
978-3-31-955329-0, 978-3-31-955330-6
|
Authors |
Christina Ising PhD, Paul T. Brinkkoetter MD, Christina Ising, Paul T. Brinkkoetter |
Editors |
Gaetano Santulli |
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. |
Mendeley readers
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Country | Count | As % |
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Unknown | 11 | 100% |
Demographic breakdown
Readers by professional status | Count | As % |
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Other | 2 | 18% |
Student > Bachelor | 2 | 18% |
Student > Ph. D. Student | 1 | 9% |
Student > Master | 1 | 9% |
Researcher | 1 | 9% |
Other | 0 | 0% |
Unknown | 4 | 36% |
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Medicine and Dentistry | 3 | 27% |
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Neuroscience | 1 | 9% |
Materials Science | 1 | 9% |
Other | 0 | 0% |
Unknown | 4 | 36% |