Fig. 4.

AIF blocks hypoxia-induced progression of PH in vitro and in vivo. A Hypoxia increased the viability of PASMCs after growth arrest for 24 h, and this effect was decreased by AIF (n = 4). B Pretreatment with an AIF overexpression plasmid blocked the effects of hypoxia on EdU incorporation in cells (n = 6). Scale bars: 50 μm. C Cell cycle analysis by flow cytometry indicated that hypoxia stimulated cell progression into G₂/M + S phase, and this effect was inhibited by AIF overexpression (n = 3). D Effects of AIF on the expression of PCNA, Cyclin A and Cyclin D under hypoxia (n = 4–5). E Represents weight ratio of the right ventricular (RV)/left ventricular (LV) + Septum (n = 6); F Represents the right ventricular systolic pressure (RVSP) from mice (n = 5); G pulmonary artery velocity time integral (PAVTI), pulmonary artery acceleration time (PAAT) and left ventricular ejection fraction (LVEF) of the hypoxic mouse model infected with AAV5-NC and AAV5-AIF (n = 6). All data are presented as the means ± standard deviation. *p < 0.05; **p < 0.01; ***p < 0.001; Nor normoxia, Hyp hypoxia, NC negative control