Key result
Adipocyte extracellular vesicles laden with oxidatively modified mitochondrial cargo induced cardiomyocyte dysfunction, which was blunted by EV inhibition or ROS scavenging.
Why the study?
Heart failure with preserved ejection fraction is increasingly prevalent in type 2 diabetes, yet disease-modifying therapies remain limited.
Does inhibition of EV biogenesis or mitochondrial ROS scavenging prevent cardiomyocyte dysfunction induced by adipocyte extracellular vesicles in T2D-HFpEF models?
Population
Patients with T2D-HFpEF and in vitro human cardiomyocytes
Design
Translational and in vitro mechanistic study
Authors
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AdEVs may link adipose stress to cardiomyocyte injury in T2D-HFpEF; hypothesis-generating for targeted therapies.
Does inhibition of EV biogenesis or mitochondrial ROS scavenging prevent cardiomyocyte dysfunction induced by adipocyte extracellular vesicles in T2D-HFpEF models?
Oxidatively modified mitochondrial cargo within adipocyte extracellular vesicles links adipose stress to cardiomyocyte dysfunction in T2D-HFpEF, highlighting novel therapeutic targets.
Ji et al. (2025) studied Type 2 diabetes-related heart failure with preserved ejection fraction. Adipocyte extracellular vesicles (AdEVs) was evaluated on Cardiomyocyte dysfunction (ROS, mitochondrial membrane potential, oxygen consumption, ATP production, apoptosis). Adipocyte extracellular vesicles laden with oxidatively modified mitochondrial cargo induced cardiomyocyte dysfunction, which was blunted by EV inhibition or ROS scavenging.
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