Publications by authors named "Ahmed A Mohsin"
Background: ER (endoplasmic reticulum) stress leads to decreased complex I activity in cardiac mitochondria. The aim of the current study is to explore the potential mechanisms by which ER stress leads to the complex I defect. ER stress contributes to intracellular calcium overload and oxidative stress that are two key factors to induce mitochondrial dysfunction.
View Article and Find Full Text PDFTransient, reversible blockade of complex I during early reperfusion after ischemia limits cardiac injury. We studied the cardioprotection of high dose of metformin in cultured cells and mouse hearts via the novel mechanism of acute downregulation of complex I. The effect of high dose of metformin on complex I activity was studied in isolated heart mitochondria and cultured H9c2 cells.
View Article and Find Full Text PDFArticle Synopsis
- Dineolignans manassantin A and B, traditionally used for ailments like edema and jaundice, target specific molecular pathways such as NF-κB and MAPK but their exact roles in therapeutic effects are still unclear.
- Recent studies have shown that manassantin inhibits mitochondrial complex I activity in mammalian cells, leading to reduced ATP levels and activation of AMP-activated protein kinase (AMPK).
- This adaptive response causes an up-regulation of aerobic glycolysis, indicating manassantin significantly affects energy metabolism and how cells utilize oxygen.