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Targeting Mitochondrial Complex I Protects Against Palmitic Acid–Induced Endothelial Dysfunction
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DOI：10.1111/dom.71164.png)
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Abstract
En 中文
Endothelial dysfunction induced by elevated free fatty acids is a critical initiating event in diabetic macrovascular complications. While mitochondrial reactive oxygen species (mtROS) are key mediators of this lipotoxic injury, the specific contribution of mitochondrial Complex I dynamics and its associated redox regulation remains to be fully elucidated.
Keywords:
endothelial dysfunction
mitochondrial complex I
oxidative stress
type 2 diabetes
Journal
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5.7
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372
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0
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