The role of PGC-1α and mitochondrial biogenesis in kidney diseases
Entity
UAM. Departamento de Medicina; Instituto de Investigación Sanitaria Fundación Jiménez Díaz (ISS-FJD); nstituto de Investigaciones Biomédicas "Alberto Sols" (IIBM)Publisher
MDPI, Basel, SwitzerlandDate
2020-02-24Citation
10.3390/biom10020347
Biomolecules 10.2 (2020): 347
ISSN
2218-273XDOI
10.3390/biom10020347Funded 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-2Editor's Version
https://doi.org/10.3390/biom10020347Subjects
Acute kidney injury; Diabetes; Kidney; Mitochondrial biogenesis; Oxidative stress; PGC-1α; Sirtuin; MedicinaRights
© 2020 The authorsAbstract
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.
Files in this item

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
This item appears in the following Collection(s)
Related items
Showing items related by title, author, creator and subject.
-
The contribution of histone crotonylation to tissue health and disease: focus on kidney health
Martínez-Moreno, Julio M.; Fontecha-Barriuso, Miguel; Martín-Sánchez, Diego; Sánchez-Niño, María D.; Ruiz-Ortega, Marta; Sanz, Ana B.; Ortiz, Alberto
2020-04-03 -
Molecular pathways driving omeprazole nephrotoxicity
Fontecha-Barriuso, Miguel; Martín-Sanchez, Diego; Martinez-Moreno, Julio M.; Cardenas-Villacres, Daniela; Carrasco, Susana; Sanchez-Niño, Maria D.; Ruiz-Ortega, Marta; Ortiz, Alberto; Sanz, Ana B.
2020-05-01