Knockdown of Sestrin2 Increases Lipopolysaccharide-Induced Oxidative Stress, Apoptosis, and Fibrotic Reactions in H9c2 Cells and Heart Tissues of Mice via an AMPK-Dependent Mechanism

<div>Schematic diagram of sesn2 functions in cardiac tissue. Sesn2 knockdown increases LPS-mediated oxidative stress, apoptosis, and fibrotic reactions in cardiomyocytes by inhibiting AMPK phosphorylation.</div>

Mediators of Inflammation

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Figure 6

Figure 6: Knockdown of Sestrin2 Increases Lipopolysaccharide-Induced Oxidative Stress, Apoptosis, and Fibrotic Reactions in H9c2 Cells and Heart Tissues of Mice via an AMPK-Dependent Mechanism 

Figure 6 | Knockdown of Sestrin2 Increases Lipopolysaccharide-Induced Oxidative Stress, Apoptosis, and Fibrotic Reactions in H9c2 Cells and Heart Tissues of Mice via an AMPK-Dependent Mechanism 