Dataset Information

Cardiomyocyte OTUD1 drives diabetic cardiomyopathy via directly deubiquitinating AMPKα2 to inhibit AMPK activity and induce mitochondrial dysfunctionCardiomyocyte OTUD1 drives diabetic cardiomyopathy via directly deubiquitinating AMPKα2 to inhibit AMPK activity and induce mitochondrial dysfunction

ABSTRACT: The sample was removed from-80℃ and melted on ice. An appropriate amount of TEAB was added to adjust pH 8.0.5 μ L of suspension was used for SDS-PAGE testing.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Permanent Cell Line Cell, Cell Culture

DISEASE(S): Type 2 Diabetes Mellitus

SUBMITTER: liu guoxuan

LAB HEAD: Xue Han

PROVIDER: PXD061479 | Pride | 2025-06-11

REPOSITORIES: Pride

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			Action	DRS
	Results.zip	Other
	XB08717DA_Flag_Slot2-34_1_36479.d.zip	Other
	XB08717DA_IgG_Slot2-33_1_36477.d.zip	Other
	checksum.txt	Txt

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Project description:Our previous studies showed that both exogenous and endogenous FGF21 inhibited cardiac apoptosis at the early stage of type 1 diabetes. Whether FGF21 induces preventive effect on type 2 diabetes-induced cardiomyopathy was investigated in the present study. High-fat-diet/streptozotocin-induced type 2 diabetes was established in both wild-type (WT) and FGF21-knockout (FGF21-KO) mice followed by treating with FGF21 for 4 months. Diabetic cardiomyopathy (DCM) was diagnosed by significant cardiac dysfunction, remodeling, and cardiac lipid accumulation associated with increased apoptosis, inflammation, and oxidative stress, which was aggravated in FGF21-KO mice. However, the cardiac damage above was prevented by administration of FGF21. Further studies demonstrated that the metabolic regulating effect of FGF21 is not enough, contributing to FGF21-induced significant cardiac protection under diabetic conditions. Therefore, other protective mechanisms must exist. The in vivo cardiac damage was mimicked in primary neonatal or adult mouse cardiomyocytes treated with HG/Pal, which was inhibited by FGF21 treatment. Knockdown of AMPKα1/2, AKT2, or NRF2 with their siRNAs revealed that FGF21 protected cardiomyocytes from HG/Pal partially via upregulating AMPK-AKT2-NRF2-mediated antioxidative pathway. Additionally, knockdown of AMPK suppressed fatty acid β-oxidation via inhibition of ACC-CPT-1 pathway. And, inhibition of fatty acid β-oxidation partially blocked FGF21-induced protection in cardiomyocytes. Further, in vitro and in vivo studies indicated that FGF21-induced cardiac protection against type 2 diabetes was mainly attributed to lipotoxicity rather than glucose toxicity. These results demonstrate that FGF21 functions physiologically and pharmacologically to prevent type 2 diabetic lipotoxicity-induced cardiomyopathy through activation of both AMPK-AKT2-NRF2-mediated antioxidative pathway and AMPK-ACC-CPT-1-mediated lipid-lowering effect in the heart.

Dataset Information

Cardiomyocyte OTUD1 drives diabetic cardiomyopathy via directly deubiquitinating AMPKα2 to inhibit AMPK activity and induce mitochondrial dysfunctionCardiomyocyte OTUD1 drives diabetic cardiomyopathy via directly deubiquitinating AMPKα2 to inhibit AMPK activity and induce mitochondrial dysfunction

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