Renal Mitochondrial ATP Transporter Ablation Ameliorates Obesity-Induced CKD.
Anna PermyakovaSharleen HamadLiad HindenSaja BaraghithyAviram Kogot-LevinOmri YosefOri ShalevManish Kumar TripathiHaitham AmalAbhishek BasuMuhammad ArifResat CinarGeorge KunosMichael BergerGil LeibowitzJoseph TamPublished in: Journal of the American Society of Nephrology : JASN (2024)
This study sheds light on the central role of adenine nucleotide translocase 2 (ANT2) in the pathogenesis of obesity-induced CKD. Our data demonstrate that ANT2 depletion in renal proximal tubule cells (RPTCs) leads to a shift in their primary metabolic program from fatty acid oxidation to aerobic glycolysis, resulting in mitochondrial protection, cellular survival, and preservation of renal function. These findings provide new insights into the underlying mechanisms of obesity-induced CKD and have the potential to be translated toward the development of targeted therapeutic strategies for this debilitating condition.
Keyphrases
- insulin resistance
- metabolic syndrome
- high glucose
- diabetic rats
- chronic kidney disease
- weight loss
- type diabetes
- oxidative stress
- weight gain
- fatty acid
- induced apoptosis
- drug induced
- adipose tissue
- machine learning
- cell cycle arrest
- cell death
- physical activity
- signaling pathway
- high intensity
- artificial intelligence