Mitochondrial Redox Signaling and Oxidative Stress in Kidney Diseases

Biomolecules

Omar Emiliano Aparicio-Trejo¹  Alfredo Cruz-Gregorio²  José Pedraza-Chaverri³  Ana Karina Aranda-Rivera³ 

[1] Departmento de Fisiopatología Cardio-Renal, Instituto Nacional de Cardiología “Ignacio Chávez”, Mexico City 14080, Mexico;Laboratorio F-225, Departamento de Biología, Facultad de Química, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico;Laboratorio F-315, Departamento de Biología, Facultad de Química, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico;

关键词: acute kidney injury (AKI);    chronic kidney disease (CKD);    tricarboxylic acid (TCA) cycle;    mitochondrial metabolism;    mitochondrial redox signaling;    mitochondrial proteins;   

DOI  :  10.3390/biom11081144

来源: DOAJ

【 摘 要 】

Mitochondria are essential organelles in physiology and kidney diseases, because they produce cellular energy required to perform their function. During mitochondrial metabolism, reactive oxygen species (ROS) are produced. ROS function as secondary messengers, inducing redox-sensitive post-translational modifications (PTM) in proteins and activating or deactivating different cell signaling pathways. However, in kidney diseases, ROS overproduction causes oxidative stress (OS), inducing mitochondrial dysfunction and altering its metabolism and dynamics. The latter processes are closely related to changes in the cell redox-sensitive signaling pathways, causing inflammation and apoptosis cell death. Although mitochondrial metabolism, ROS production, and OS have been studied in kidney diseases, the role of redox signaling pathways in mitochondria has not been addressed. This review focuses on altering the metabolism and dynamics of mitochondria through the dysregulation of redox-sensitive signaling pathways in kidney diseases.

【 授权许可】

Unknown