ABSTRACT
This chapter's focus is on epigenetics because epigenetic mechanisms regulate the magnitude and timing of gene expression in a cell-specific way, and therefore the resulting transcriptomes. Evidence presented in this chapter shows that DNA methylation, histone post-translational modifications, and ncRNAs are important players in the pathogenesis of pulmonary artery hypertension (PAH) or the prevention of PAH. However, no effective treatment for PAH exists. In this regard, exciting epigenetic-based therapies are being developed for cancers. Because PAH shares common pathological processes of increased cell proliferation and cell cycling, enhanced cell migration, and decreased cell apoptosis with cancer biology, innovative treatment opportunities may become possible to intervene in patients who would otherwise develop persistent PAH and its long-term consequence of right ventricle hypertrophy and ultimately dysfunction and failure. However, important gaps in the field remain, some of which are addressed in this chapter. A caveat is that the field is advancing quickly so new processes and molecular players are coming into focus, which are not included in this chapter. Although gaps in knowledge exist, the field has the exciting prospect of innovative studies to come that will test efficacy, in the context of PAH, of new therapeutics.
