Journal
BIOMOLECULES
Volume 9, Issue 9, Pages -Publisher
MDPI
DOI: 10.3390/biom9090404
Keywords
fasting; fibrosis; mitochondrial dysfunction; oxidative stress; inflammation; ER stress; ischemia-reperfusion injury
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Funding
- Consejo Nacional de Ciencia y Tecnologia (CONACyT-Mexico) [A1-S-7496]
- Programa de Apoyo a Proyectos de Investigacion e Innovacion Tecnologica (PAPIIT-Mexico) [IN202219]
- Programa de Apoyo a la Investigacion y Posgrado (PAIP-Mexico) [5000-9105]
- Fondos del Gasto Directo autorizado a la Subdireccion de Investigacion Basica, Instituto Nacional de Cardiologia Ignacio Chavez
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Ischemia-reperfusion injury of the kidney may lead to renal fibrosis through a combination of several mechanisms. We recently demonstrated that fasting protects the rat kidney against oxidative stress and mitochondrial dysfunction in early acute kidney injury, and also against fibrosis development. Here we show that preoperative fasting preserves redox status and mitochondrial homeostasis at the chronic phase of damage after severe ischemia. Also, the protective effect of fasting coincides with the suppression of inflammation and endoplasmic reticulum stress, as well as the down-regulation of the mechanistic target of rapamycin (mTOR) and extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathways in the fibrotic kidney. Our results demonstrate that fasting targets multiple pathophysiological mechanisms to prevent renal fibrosis and damage that results after renal ischemia-reperfusion injury.
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