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• W4376271664 abstract "Abstract Mitochondria are intracellular organelles that regulate cell survival and death, and hyperglycemia modulates mitochondrial function in endothelial cells. In the current study, we have discovered that high glucose (HG) treatment reduces FUNDC1 ( FUN14 domain containing 1 ) expression in endothelial cells. FUNDC1 expression in mitochondria inhibits proteasomal degradation of COX-IV, and regulates mitochondrial complexes I and IV activity and ATP synthesis. FUNDC1 depletion in HG affects mitochondrial complexes I and IV activity and ATP synthesis and promotes mitochondrial damage through loss of mitochondrial membrane potential and ROS (Reactive Oxygen Species) production. BAM15, a mitochondrial uncoupler, improves mitochondrial function and endothelial survival more effectively. Co-treatment of HG with BAM15 increased FUNDC1 protein expression, mitochondrial translocation of FUNDC1 in HG-treated cells. BAM15-induced up regulation of FUNDC1 expressions improve mitochondrial expression of COX-IV, and complex I and IV activity and ATP synthesis. Our findings propose that FUNDC1 expression in endothelial cells under hyperglycemic stress play a significant role in limiting vascular damage and apoptotic cell death." @default.
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• W4376271664 date "2023-05-12" @default.
• W4376271664 modified "2023-09-30" @default.
• W4376271664 title "BAM15, a mitochondrial uncoupler regulates mitochondrial function by FUNDC1 dependently in hyperglycemia" @default.
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• W4376271664 doi "https://doi.org/10.21203/rs.3.rs-2903880/v1" @default.
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