Targeting Molecular and Cellular Mechanisms in Pulmonary Hypertension

Pulmonary hypertension (PH) is described as an elevated mean pulmonary artery pressure (mPAP) of 25 mmHg or above, measured at rest by right-heart catheterization. The precise worldwide occurrence of PH is not easily measured, majorly as a result of its complex etiology, and its progression is likely to be underestimated. Extensive reports on the pathophysiology of PH and incidence etiology at the cellular and molecular level have been well documented. In addition, basic clinical research studies have shown promising potentials of popular and widely known cardiovascular biomarkers, but with limited clinical significance in the management and diagnosis of PH as a result of decreased specificity as well as several other cardiovascular complications of patients with PH. Conversely, a large panel of experimental research studies reveal novel cellular and molecular mechanisms, drug targets, and biomarkers following the principle of the evidence-based medicine. Unfortunately, the basic extrapolation of these finding results to clinical practice is not straightforward because of large complex nature of the pathophysiology of PH. Hence, there is the need for more translational medicine research to fully comprehend the pathophysiological classification of PH and define accurately its biomarkers and therapeutic approach for PH treatment. We discuss in this chapter the types of PH, the novel therapeutic options available, and the molecular mechanism behind PH and its possible drug targets for treatments at the cellular and molecular level. Several factors like oxidative stress, cell signaling, inflammation, and mechanisms of immune systems are highlighted that may be responsible for the pathophysiology of PH and its complications. Each of these processes is discussed separately, for clarity purpose, but most importantly, crucial cross functions will occur among the pathways in PH patients.