4.6 Article

Expression Profiles of Kidney Mitochondrial Proteome during the Progression of the Unilateral Ureteral Obstruction: Focus on Energy Metabolism Adaptions

Journal

METABOLITES
Volume 12, Issue 10, Pages -

Publisher

MDPI
DOI: 10.3390/metabo12100936

Keywords

unilateral ureteral obstruction (UUO); kidney fibrosis; mitochondria proteome; energy metabolism

Funding

  1. Consejo Nacional de Ciencia y Tecnologia (CONACyT) [A1-S-7495]
  2. Programa de Apoyo a Proyectos de Investigacion e Innovacion Tecnologica of Universidad Nacional Autonoma de Mexico (UNAM) [IN200922]
  3. Programa de Apoyo a la Investigacion y el Posgrado of Facultad de Quimica, UNAM [5000-9105]

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The study examined the impact of UUO at different time points on the mitochondrial proteome of rat kidneys, revealing changes in proteins related to oxidative phosphorylation, the tricarboxylic acid cycle, and fatty acid metabolism, all of which are associated with bioenergetics during ON.
Kidney diseases encompass many pathologies, including obstructive nephropathy (ON), a common clinical condition caused by different etiologies such as urolithiasis, prostatic hyperplasia in males, tumors, congenital stenosis, and others. Unilateral ureteral obstruction (UUO) in rodents is an experimental model widely used to explore the pathophysiology of ON, replicating vascular alterations, tubular atrophy, inflammation, and fibrosis development. In addition, due to the kidney's high energetic demand, mitochondrial function has gained great attention, as morphological and functional alterations have been demonstrated in kidney diseases. Here we explore the kidney mitochondrial proteome differences during a time course of 7, 14, and 21 days after the UUO in rats, revealing changes in proteins involved in three main metabolic pathways, oxidative phosphorylation (OXPHOS), the tricarboxylic acid cycle (TCA), and the fatty acid (FA) metabolism, all of them related to bioenergetics. Our results provide new insight into the mechanisms involved in metabolic adaptations triggered by the alterations in kidney mitochondrial proteome during the ON.

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