Publications by authors named "R Undamatla"
Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum of pathologies that includes steatosis, steatohepatitis (NASH) and fibrosis and is strongly associated with insulin resistance and type 2 diabetes. Changes in mitochondrial function are implicated in the pathogenesis of NAFLD, particularly in the transition from steatosis to NASH. Mitophagy is a mitochondrial quality control mechanism that allows for the selective removal of damaged mitochondria from the cell via the autophagy pathway.
View Article and Find Full Text PDFNonalcoholic fatty liver disease (NAFLD) encompasses a spectrum of pathologies that includes steatosis, steatohepatitis (NASH) and fibrosis and is strongly associated with insulin resistance and type 2 diabetes. Changes in mitochondrial function are implicated in the pathogenesis of NAFLD, particularly in the transition from steatosis to NASH. Mitophagy is a mitochondrial quality control mechanism that allows for the selective removal of damaged mitochondria from the cell via the autophagy pathway.
View Article and Find Full Text PDFArticle Synopsis
- PARKIN is crucial for maintaining mitochondrial health through mitophagy, and its loss in the liver is linked to worsening fatty liver disease associated with obesity.
- Mice with liver-specific knockout of the Prkn gene (LKO) showed a significant increase in liver fat (45%) on a high-fat diet, despite no changes in overall body weight or fat levels compared to control mice.
- Analysis of liver tissues revealed reduced mitochondrial function and significant alterations in gene expression related to lipid metabolism and fibrosis in LKO mice under high-fat dietary conditions.