Dysregulation of the Mitochondrial Proteome Occurs in Mice Lacking Adiponectin Receptor 1.

Decreased serum adiponectin levels in type 2 diabetes has been linked to the onset of mitochondrial dysfunction in diabetic complications by impairing AMPK-SIRT1-PGC-1α signaling via impaired adiponectin receptor 1 (AdipoR1) signaling. Here, we aimed to characterize the previously undefined role of disrupted AdipoR1 signaling on the mitochondrial protein composition of cardiac, renal, and hepatic tissues as three organs principally associated with diabetic complications. Comparative proteomics were performed in mitochondria isolated from the heart, kidneys and liver of mice.

Myocardial mitochondrial dysfunction in mice lacking adiponectin receptor 1.

Hypoadiponectinemia is an independent predictor of cardiovascular disease, impairs mitochondrial function in skeletal muscle, and has been linked to the pathogenesis of Type 2 diabetes. In models of Type 2 diabetes, myocardial mitochondrial function is impaired, which is improved by increasing serum adiponectin levels. We aimed to define the roles of adiponectin receptor 1 (AdipoR1) and 2 (AdipoR2) in adiponectin-evoked regulation of mitochondrial function in the heart.

Impact of chronic kidney disease on long-term clinical outcomes after percutaneous coronary intervention with drug-eluting or bare-metal stents.

Chronic kidney disease (CKD) is associated with adverse outcomes after coronary bare-metal stent (BMS) and drug-eluting stent (DES) implantation, but it is unclear which stent type is associated with lower risk for morbidity and mortality in this population. Uniform treatment standards during coronary stent implantation and a median follow-up period of 2.8 years characterize the FReIburg STent (FRIST) registry, designed as a long-term outcome evaluation of a single tertiary referral cardiovascular center.