Reducing TRPC1 Expression through Liposome-Mediated siRNA Delivery Markedly Attenuates Hypoxia-Induced Pulmonary Arterial Hypertension in a Murine Model

Figure 11

Proposed mechanisms underlying the therapeutic actions of TRPC1 knockdown via Lipofectamine delivered siRNA against hypoxia-induced pulmonary arterial hypertension (PAH) in a murine model of pulmonary arterial hypertension (PAH). α-SMA: alpha-smooth muscle actin; BMP-2: bone morphogenetic protein-2; c-Csp3: cleaved caspase-3; c-PARP: cleaved poly(ADP-ribose) polymerase; eNOS: endothelial nitric oxide synthase; ET-1: endothelin-1; HIF-1α: hypoxia-inducible factor 1-alpha; HW: heart weight; MHC: myosin heavy chain; mito-Bax: mitochondrial Bax; MMP-9: matrix metalloproteinase-9; p-Smad: phosphorylated Smad; RVSP: right ventricle systolic pressure; TGF-β: transforming growth factor beta; TNF-α: tumor necrosis factor alpha; TRPC: transient receptor potential cation channel; VEGF: vascular endothelial growth factor.