Fig. 3

Elevated ROS can exacerbate the development of PAH, AS and MI, and inhibition of ROS expression can slow down the development of PAH, AS and MI. A OS promoted the development of PAH, as seen by the proliferation of PAECs and PASMCs promoting vascular remodeling compared to normal vascular architecture. NOXs and their associated signaling pathways contribute to the development of PAH, such as the NOX1/ROS/Nfr2x signaling pathway that activates and promotes OS to exacerbate disease development. In addition, HIF1α and NDUFA4L2 under hypoxic conditions promote cell proliferation exacerbating disease progression. B There is lipid and/or fiber accumulation in the AS vessels compared to normal vessels (visible as a gray-brown fraction), a process facilitated by OS. In addition, AS as a chronic inflammatory disease, there is crosstalk between OS-related and inflammatory signaling pathways during the development, for example, NOXs exacerbate the development of AS and perivascular inflammatory response, and the inflammatory response further drives the overproduction of ROS in an interactive process. In this process, the NF-κB signaling pathway deserves to be focused on. In addition, XO also serves as an important source of ROS to drive the development of AS. (C) Cardiomyocyte death and fibrous scarring were observed in MI compared to normal cardiomyocytes. NOXs are involved in promoting the process of myocardial injury. Large amounts of ROS are also produced after MI, further exacerbating cardiomyocyte death. Notably, NOX4 may reduce the protective effect of inflammation on cardiomyocytes. In addition, MAO induced increased ROS expression and exacerbated MI. Finally, increasing the bioavailability of NO can reduce the expression of ROS and slow down the development of PAH, AS and MI