TLR4 Activation Promotes the Progression of Experimental Autoimmune Myocarditis to Dilated Cardiomyopathy by Inducing Mitochondrial Dynamic Imbalance

Figure 7

Intervening OMA1 and YME1L suppressed mitochondrial fission and apoptosis in H9C2. (a-b) Representative immunoblots of OMA1, YME1L, and OPA1 in H9C2 treated with TNF-α and H₂O₂. (c-d) The effect of OMA1 knockdown on the level of YMEL1 and OPA1 in H9C2 treated with TNF-α and H₂O₂. (e) The effect of YME1L overexpression on the level of YMEL1 and OPA1 in H9C2 treated with TNF-α and H₂O₂. (f-g) Quantification of four independent experiments for mitochondrial morphology in H9C2 treated with TNF-α and H₂O₂. (h) The effect of OMA1 knockdown or YME1L overexpression on apoptosis in H9C2 treated with TNF-α and H₂O₂ with flow cytometry (). versus control; , versus H9C2 treated with TNF-α or H₂O₂ group; versus H9C2 treated with TNF-α or H₂O₂ group.

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