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

Figure 1

Mfn2 was downregulated in rat heart tissues with TAC surgery and in cardiac fibroblasts treated with TGF-β1. Rats were divided into two groups: sham and TAC. (a) Cardiac image and cardiac hypertrophy index, HW/BW (); (b) the mRNA and protein levels of CTGF, TGF-β, collagen1, and α-SMA in rat heart tissues (); (c) the mRNA and protein levels of Mfn2 in rat heart tissues (); cardiac fibroblasts were divided into two groups: control and TGF-β1 treatment: (d) the mRNA and protein levels of CTGF, TGF-β, and α-SMA in the process of cardiac fibroblast activation (); (e) immunofluorescence staining of α-SMA in cardiac fibroblasts (the red fluorescence indicated α-SMA and the blue fluorescence indicated the cell nucleus stained by DAPI, ); (f) the proliferation rate of cells (the red fluorescence indicated EdU-incorporated cells and the blue fluorescence indicated the cell nucleus stained by DAPI, ); (g) the migration activity of cardiac fibroblasts (determined by the number of protruding cells from the wound border); (h) the mRNA and protein levels of Mfn2 in the process of cardiac fibroblast activation (). Data in (a–h) are expressed as . indicates , indicates , and indicates vs. the sham or control groups.

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