Key result
Ulk1-Rab9-dependent alternative mitophagy is activated during chronic high-fat diet consumption and protects the heart against obesity-associated cardiomyopathy.
Why the study?
General autophagic flux declines after 6 weeks of high-fat diet consumption, leaving unclear whether mitophagy remains active during chronic obesity-associated cardiomyopathy.
Population
Mice fed a normal diet or high-fat diet (including ulk1 knockout, Rab9 S179A knock-in, and Rab9 overexpression models)
Comparison
High-fat diet (60 kcal% fat) vs normal diet and genetic mitophagy manipulations vs controls
Design
Preclinical animal study
Follow-up
At least until 24 weeks
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Alternative mitophagy may preserve cardiac function in chronic obesity cardiomyopathy models; leaves open whether Ulk1-Rab9 pathways warrant therapeutic targeting in patients.
Ulk1-Rab9-dependent alternative mitophagy serves as a crucial compensatory mechanism to protect the heart against obesity-associated cardiomyopathy during chronic high-fat diet consumption.
A 2021 study studied Obesity-associated cardiomyopathy. High-fat diet (HFD) and genetic modifications (ulk1 knockout, Rab9 S179A knock-in, Rab9 overexpression) vs. Normal diet and control mice was evaluated on Mitophagy activation and cardiac function. Ulk1-Rab9-dependent alternative mitophagy is activated during chronic high-fat diet consumption and protects the heart against obesity-associated cardiomyopathy.
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