RÉSUMÉ
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.
Sujet(s)
Atteinte rénale aigüe/métabolisme , Mitochondries/métabolisme , Stress oxydatif , Maturation post-traductionnelle des protéines , Espèces réactives de l'oxygène/métabolisme , Insuffisance rénale chronique/métabolisme , Atteinte rénale aigüe/génétique , Atteinte rénale aigüe/anatomopathologie , Apoptose/génétique , Acides gras/métabolisme , Humains , Rein/métabolisme , Rein/anatomopathologie , Mitochondries/génétique , Mitochondries/anatomopathologie , Dynamique mitochondriale , Mitophagie/génétique , NADPH Oxidase 1/génétique , NADPH Oxidase 1/métabolisme , Facteur de transcription NF-kappa B/génétique , Facteur de transcription NF-kappa B/métabolisme , Phosphorylation oxydative , Insuffisance rénale chronique/génétique , Insuffisance rénale chronique/anatomopathologie , Transduction du signal , Superoxide dismutase/génétique , Superoxide dismutase/métabolismeRÉSUMÉ
Malignant conversion of cancer cells requires efficient mitochondria reprogramming orchestrated by hundreds of genes. The transformation includes increased energy demand, biosynthesis of precursors, and reactive oxygen species needed to accelerate cell growth, proliferation, and survival. Reprogramming involves complex gene alterations that have not been methodically curated. Therefore, we systematically analyzed the literature of cancer-related genes in mitochondria. Through the analysis of >2500 PubMed abstracts and >1600 human genes, we identified 228 genes showing clear roles in cancer. Each gene was classified according to their homeostatic function, together with the pathological transitions that contribute to specific cancer hallmarks. The potential clinical relevance of these hallmarks and genes is discussed by representative examples and validated by detecting differences in gene expression levels across 16 different types of cancer. A compendium, including the gene functions and alterations underpinning cancer progression, can be explored at http://bioinformatica.mty.itesm.mx/MitoCancer.