Oxidative Medicine and Cellular Longevity / 2019 / Article / Fig 3

Research Article

Inhibition of Mitofusin-2 Promotes Cardiac Fibroblast Activation via the PERK/ATF4 Pathway and Reactive Oxygen Species

Figure 3

Mitochondrial morphology was impaired in activated cardiac fibroblasts. (a) MitoTracker analysis of cardiac fibroblasts treated with TGF-β1 for 24 h; (b) the morphology of fused and fragmented mitochondria in cardiac fibroblasts treated with TGF-β1 for 24 h; (c) the morphology of fused and fragmented mitochondria in cardiac fibroblasts with siMfn2 transfection in the presence or absence of TGF-β1; (d) the morphology of fused and fragmented mitochondria in cardiac fibroblasts with overexpression adenovirus transduction in the presence or absence of TGF-β1; data in (a–d) are expressed as . The red arrow is for fused mitochondria; the yellow arrow is for fragmented mitochondria; indicates , indicates , and indicates vs. the NC or NC+TGF-β1 groups.
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