Molecular Characterization of Reactive Oxygen Species in Systemic and Pulmonary Hypertension

Abstract

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.

MicroRNA-143 Activation Regulates Smooth Muscle and Endothelial Cell Crosstalk in Pulmonary Arterial Hypertension

“…Indeed, hypoxia itself can clearly induce the expression of the cluster. This is in keeping with the fact that approximately 20% of hypoxia-induced transcripts are for non-coding RNA 32 , in line with the role of chronic hypoxia and reactive oxygen species in the development of pulmonary hypertension 33 . In addition, we assessed the impact of TGF-β signalling on this novel promoter region.…”

Leukotriene B 4 Activates Pulmonary Artery Adventitial Fibroblasts in Pulmonary Hypertension

“…47 Elevated ROS lead to vascular remodeling and increased PA pressures in PH. 29, 43, 48, 49 Nox is one of the major sources of cellular ROS known to be pathogenic in PAH, 2, 27–29 and Nox4 is the most important isoform of Nox in adventitial fibroblasts. Nox4 positive fibroblasts were increased in PH lungs (Figure 5B) as were Nox4/5-LO double positive fibroblasts.…”

Sevoflurane postconditioning protects the myocardium against ischemia/reperfusion injury via activation of the JAK2–STAT3 pathway

“…Reactive oxygen species are involved in many diseases, including neurological diseases (Zuo et al, 2015b), heart failure (Zuo et al, 2015a) and hypertension (Zuo et al, 2014b). A large number of studies have shown that ischemic postconditioning can significantly reduce ROS production, thereby reducing myocardial I/R injury (Barsukevich et al, 2015; Singh et al, 2012; Zhao et al, 2003).…”