The role of PGC-1α and mitochondrial biogenesis in kidney diseases
Entidad
Instituto de Investigación Sanitaria Fundación Jiménez Díaz (IIS-FJD); Instituto de Investigaciones Biomédicas "Alberto Sols" (IIBM); UAM. Departamento de MedicinaEditor
MDPI, Basel, SwitzerlandFecha de edición
2020-02-24Cita
10.3390/biom10020347
Biomolecules 10.2 (2020): 347
ISSN
2218-273XDOI
10.3390/biom10020347Financiado por
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.)Proyecto
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-2Versión del editor
https://doi.org/10.3390/biom10020347Materias
Acute kidney injury; Diabetes; Kidney; Mitochondrial biogenesis; Oxidative stress; PGC-1α; Sirtuin; MedicinaDerechos
© 2020 The authorsResumen
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.
Lista de ficheros
Google Scholar:Fontecha-Barriuso, Miguel
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Martin-Sanchez, Diego
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Martinez-Moreno, Julio Manuel
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Monsalve, Maria
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Ramos, Adrian Mario
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Sánchez Niño, María Dolores
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Ruiz Ortega, Marta
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Ortiz Arduán, Alberto
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Sanz, Ana Belen
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