The role of redox signaling in mitochondria and endoplasmic reticulum regulation in kidney diseases


Por: Aparicio-Trejo, OE, Hernandez-Cruz, EY, Reyes-Fermin, LM, Ceja-Galicia, ZA, Pedraza-Chaverri, J

Publicada: 1 may 2025 Ahead of Print: 1 abr 2025
Resumen:
Kidney diseases are among the fastest worldwide growing pathologies. This growth together with their high mortality rate emphasizes the importance of generating vital information about the mechanism involved in their pathophysiology to determine possible therapeutic targets. Recently, mitochondrial damage and their implication in the reactive oxygen spices (ROS) signaling and redox homeostasis have emerged as a hub point in the pathologic mechanism involved in renal pathologies. ROS in low levels are necessary to maintain cell processes as well as the mitochondria homeostasis and its association with other organelles, especially the with the endoplasmic reticulum (ER). However, the information about how redox signaling interacts and interferes with other cellular processes and the mechanism involved has not been fully integrated. Furthermore, in higher concentrations, these ROS promotes pathologic pathways linked to renal disease progression like, mitochondrial biogenesis reduction, ER stress, calcium overload, inflammation, cell death and fibrosis. Therefore, the aim of this review is to describe the molecular mechanisms involved in the redox signaling influence on mitochondrial and ER homeostasis, focusing on lipid metabolism and ss-oxidation, mitochondrial biogenesis, inflammations, ER stress and calcium homeostasis, as well as the effects of these alteration in the genesis and development of renal disease, with emphasis in acute kidney injury (AKI) and chronic kidney disease (CKD).

Filiaciones:
Aparicio-Trejo, OE:
 Natl Inst Cardiol Ignacio Chavez, Dept Cardiorenal Physiopathol, Mexico City 14080, Mexico

Hernandez-Cruz, EY:
 Univ Nacl Autonoma Mexico, Fac Chem, Dept Biol, Lab F 315, Mexico City, Mexico

Reyes-Fermin, LM:
 Univ Nacl Autonoma Mexico, Fac Chem, Dept Biol, Lab F 315, Mexico City, Mexico

Ceja-Galicia, ZA:
 Natl Inst Cardiol Ignacio Chavez, Dept Cardiovasc Biomed, Mexico City 14080, Mexico

Pedraza-Chaverri, J:
 Univ Nacl Autonoma Mexico, Fac Chem, Dept Biol, Lab F 315, Mexico City, Mexico
ISSN: 03405761
Editorial
Springer-Verlag, TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY, Alemania
Tipo de documento: Review
Volumen: 99 Número: 5
Páginas: 1865-1891
WOS Id: 001464428200001
ID de PubMed: 40214774