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The role of PGC-1α and mitochondrial biogenesis in kidney diseases

Author
Fontecha-Barriuso, Miguel; Martin-Sanchez, Diego; Martinez-Moreno, Julio Manuel; Monsalve, Maria; Ramos, Adrian Mario; Sanchez-Niño, Maria Dolores; Ruiz-Ortega, Marta; Ortiz, Alberto; Sanz, Ana Belen
Entity
UAM. Departamento de Medicina; Instituto de Investigación Sanitaria Fundación Jiménez Díaz (ISS-FJD); nstituto de Investigaciones Biomédicas "Alberto Sols" (IIBM)
Publisher
MDPI, Basel, Switzerland
Date
2020-02-24
Citation
10.3390/biom10020347
Biomolecules 10.2 (2020): 347
 
 
 
ISSN
2218-273X
DOI
10.3390/biom10020347
Funded by
Supported by ISCIII-FIS, FEDER funds, CP14/00133, PI16/02057, PI16/01900, PI18/01366, PI19/00588, PI19/00815, DTS18/00032, ERA-PerMed-JTC2018 (KIDNEY ATTACK AC18/00064 and PERSTIGAN AC18/00071, ISCIII-RETIC REDinREN RD016/0009, Sociedad Española de Nefrología, Fundacion Renal Iñigo Álvarez de Toledo (FRIAT), ISCIII Miguel Servet (A.B.S., M.D.S.-N.), ISCIII Sara Borrell (J.M.M.-M.), Comunidad de Madrid CIFRA2 B2017/BMD-3686 (M.F.-B. and D.M.-S.)
Project
Gobierno de España. CP14/00133; Gobierno de España. PI16/02057; Gobierno de España. PI16/01900; Gobierno de España. PI18/01366; Gobierno de España. PI19/00588; Gobierno de España. PI19/00815; Gobierno de España. DTS18/00032; info:eu-repo/grantAgreement/EC/H2020/78590/EU//ERA-PerMed; Gobierno de España. RD016/0009; Comunidad de Madrid. B2017/BMD-3686/CIFRA-2
Editor's Version
https://doi.org/10.3390/biom10020347
Subjects
Acute kidney injury; Diabetes; Kidney; Mitochondrial biogenesis; Oxidative stress; PGC-1α; Sirtuin; Medicina
URI
http://hdl.handle.net/10486/693405
Rights
© 2020 The authors

Licencia Creative Commons
Esta obra está bajo una Licencia Creative Commons Atribución 4.0 Internacional.

Abstract

Chronic kidney disease (CKD) is one of the fastest growing causes of death worldwide, emphasizing the need to develop novel therapeutic approaches. CKD predisposes to acute kidney injury (AKI) and AKI favors CKD progression. Mitochondrial derangements are common features of both AKI and CKD and mitochondria-targeting therapies are under study as nephroprotective agents. PGC-1α is a master regulator of mitochondrial biogenesis and an attractive therapeutic target. Low PGC-1α levels and decreased transcription of its gene targets have been observed in both preclinical AKI (nephrotoxic, endotoxemia, and ischemia-reperfusion) and in experimental and human CKD, most notably diabetic nephropathy. In mice, PGC-1α deficiency was associated with subclinical CKD and predisposition to AKI while PGC-1α overexpression in tubular cells protected from AKI of diverse causes. Several therapeutic strategies may increase kidney PGC-1α activity and have been successfully tested in animal models. These include AMP-activated protein kinase (AMPK) activators, phosphodiesterase (PDE) inhibitors, and anti-TWEAK antibodies. In conclusion, low PGC-1α activity appears to be a common feature of AKI and CKD and recent characterization of nephroprotective approaches that increase PGC-1α activity may pave the way for nephroprotective strategies potentially effective in both AKI and CKD.
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Google™ Scholar:Fontecha-Barriuso, Miguel - Martin-Sanchez, Diego - Martinez-Moreno, Julio Manuel - Monsalve, Maria - Ramos, Adrian Mario - Sanchez-Niño, Maria Dolores - Ruiz-Ortega, Marta - Ortiz, Alberto - Sanz, Ana Belen

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  • Producción científica en acceso abierto de la UAM [14677]

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Universidad Autónoma de Madrid. Biblioteca
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