Mitochondrial Reactive Oxygen Species in Lipotoxic Hearts Induces Post-Translational Modifications of AKAP121, DRP1 and OPA1 That Promote Mitochondrial Fission
نویسندگان
چکیده
Kensuke Tsushima1,2*, Heiko Bugger2,3*, Adam R. Wende2,4, Jamie Soto1,2, Gregory A. Jenson1, Austin R. Tor1, Rose McGlauflin1, Helena C. Kenny1, Yuan Zhang1, Rhonda Souvenir1, Xiao X. Hu2, Crystal L. Sloan2, Renata O. Pereira1, Vitor A Lira5, Kenneth W. Spitzer6, Terry L. Sharp7, Kooresh I. Shoghi7, Genevieve C. Sparagna8, Eva A. Rog-Zielinska9, Peter Kohl9, Oleh Khalimonchuk10,11, Jean E. Schaffer12, E. Dale Abel1,2
منابع مشابه
Mitochondrial Reactive Oxygen Species in Lipotoxic Hearts Induce Post-Translational Modifications of AKAP121, DRP1, and OPA1 That Promote Mitochondrial Fission.
RATIONALE Cardiac lipotoxicity, characterized by increased uptake, oxidation, and accumulation of lipid intermediates, contributes to cardiac dysfunction in obesity and diabetes mellitus. However, mechanisms linking lipid overload and mitochondrial dysfunction are incompletely understood. OBJECTIVE To elucidate the mechanisms for mitochondrial adaptations to lipid overload in postnatal hearts...
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Diabetic cardiomyopathy is associated with cardiac lipotoxicity and mitochondrial dysfunction, and a better understanding of the mechanisms involved are needed. To examine the mechanisms linking lipid overload and diabetic cardiomyopathy, Tsushima et al studied a mouse model with overexpression of ACSL1 (long-chain acyl-CoA synthetase 1) in cardiomyocytes (ACS-transgenic [Tg]). ACSL1 was under ...
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