LAUSR

M icroRNAs (miRNAs) have emerged as key determinants of health and disease by mediating gene expression in response to homeostatic or pathogenic stimuli. Considerable advances in miRNA biology have revealed that many miRNAs are expressed in a cell type–specific manner and may be transiently or chronically downregulated or upregulated before, at, or after disease inception or coincident with disease progression. MiRNAs participate in intracellular and intercellular signaling and can be released to circulate in the bloodstream, positioning them as ideal candidate biomarkers.1 The 2 aforementioned concepts are indicative of the temporal and spatial actions of miRNAs that are relevant for any disease process. In pulmonary hypertension, in vitro and preclinical studies have implicated several miRNAs in the mechanisms underlying the disease pathobiology. MiRNAs function as disease modifiers by altering levels vasoactive compounds, shifting metabolism towards glycolysis, dysregulating mitochondrial function, or stimulating cell proliferation and migration to promote vascular remodeling, a precursor to aberrant hemodynamic profiles as well as right ventricular dysfunction and failure (reviewed in2,3). Therefore, a role for miRNAs in modulating the pulmonary vascular disease phenotype is well defined; however, which population of miRNAs (in situ, intercellular, or circulating) are responsible for these pathophenotypic changes remains incompletely characterized.