Diabetic Kidney Disease Susceptibility: Endothelial Mitochondrial Dysfunction as Essential Mediator

What is it about?

The article discusses the identification of mitochondrial-dependent glomerular endothelial pathomechanisms as essential in mediating experimental diabetic nephropathy in DKD-susceptible mice. The study suggests that DKD susceptibility in mice and human DKD is characterized by an essential role of endothelial injury and dysfunction with loss of fenestrations, mediated partly by EDNRA-induced endothelial mtStress. The findings indicate that increased urinary 8-oxodG excretion was characteristic of patients with diabetes with progressive chronic kidney disease. The article also suggests that antagonism of the pluripotent EDN1 signaling system and in particular the cognate receptor EDNRA has emerged as a promising therapeutic strategy in cardiovascular and renal diseases, including DKD. [Some of the content on this page has been created by AI]

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Why is it important?

This research is important because it identifies a key pathway that contributes to the development of diabetic kidney disease (DKD) in susceptible individuals. The study highlights the role of endothelial cell injury and dysfunction, which is mediated by the EDNRA-induced mitochondrial dysfunction and oxidative stress. This finding may provide a common pathomechanism underlying the initiation and progression of DKD in humans. Key Takeaways: 1. Mitochondrial-dependent glomerular endothelial pathomechanisms are essential in mediating experimental diabetic nephropathy in DKD-susceptible mice. 2. DKD susceptibility in mice and human DKD is characterized by an essential role of endothelial injury and dysfunction with loss of fenestrations, mediated partly by EDNRA-induced endothelial mtStress. 3. The study suggests an essential role for endothelial cell injury in orchestrating the characteristic glomerular response and lesions of DKD, in particular podocyte injury/depletion, glomerular basement membrane alterations, and mesangial expansion.