Research Article
Inhibition of Mitofusin-2 Promotes Cardiac Fibroblast Activation via the PERK/ATF4 Pathway and Reactive Oxygen Species
Figure 6
Schematic representation of the PERK/ATF4/ROS pathways through which Mfn2 inhibition triggers cardiac fibroblast activation. Upon pathological stimuli, gene silencing of Mfn2 reduced OMM Mfn2 expression, resulting in elevated expression levels of the PERK/ATF4 branch, and the generation of ROS ultimately leading to cardiac fibroblast activation.