Microarray studies in pulmonary arterial hypertension

Microarray studies have been performed on lung tissue, freshly isolated circulating cells and cells cultured from patients with idiopathic, hereditary and secondary forms of pulmonary arterial hypertension (PAH). These studies have provided a wealth of information on the characteristics of end-stage disease, but information about the origin of disease is only clear in hindsight. The central conclusions that can be drawn from these studies are that end-stage disease includes a massive but currently poorly defined inflammatory response, induction of angiogenesis genes for an as yet remaining unknown purpose, suppression of the BMP pathway even in idiopathic and secondary cases, and a host of more subtle changes, including mitochondrial and actin organisation changes. Moreover, the same physiologic endpoints can be achieved through use of any of multiple genes, and so specific genes are usually less important than the pathways they lie in; the exception to this rule must lie in as yet undefined critical nodes. Finally, the lack of consistency in methodologies of analysis makes cross-experiment comparisons difficult, and likely means that there is data collected in these studies that await interpretation.