Molecular characterization of reactive oxygen species in systemic and pulmonary hypertension.

Hypertension, commonly recognized as high blood pressure, is a serious disease that affects millions of people worldwide. Similar to many physiological disorders, hypertension consists of several different cellular signaling pathways that involve various molecular messengers. Recent studies have shown that reactive oxygen species (ROS) play a substantial role in the development of both systemic and pulmonary hypertension, contributing to the pathology of this disease. However, the exact molecular mechanism of ROS in hypertension is not completely understood. In this review, we extensively examine and discuss the most recent experimental findings regarding the role of ROS in both pulmonary and systemic hypertension. Current studies show that excessive ROS not only promote JAK/STAT (janus kinase/signal transducers and activators of transcription)-mediated vascular remodeling in an angiotensin (ANG) II-induced hypertension model but also decrease the nitric oxide bioavailability. Furthermore, it has been shown that ROS generation can be mitigated through the inhibition of upstream ANG II or by blocking key ROS generators, such as nicotinamide adenine dinucleotide phosphate oxidase. Thus, various treatment options have been explored. Yet, as discussed in the current review, the regulation of ROS via novel antioxidant therapies may provide an alternative treatment for hypertension in the future.