Similarly, compared with Ad-EV treatment, Sp1 overexpression or Ndufs1 overexpression attenuated hypoxia-induced elevation in intracellular oxidation levels, the level of fibrotic markers, and the level of HF markers in NRCMs, whereas the protective effect of Sp1 was inhibited by Ndufs1 knockdown, as evidenced by GSH levels, GPx activity, and the mRNA levels of Col1a1, Col3a1, ANP, and BNP (Fig. 7d–h). The gene discussed is SP1; the disease is hydrops fetalis.