Menon S, Fessel J, West J
Pulmonary Vascular Research Institute, Jawaharlal Nehru University, New Delhi, India.
Int J Clin Pract Suppl. 2011 Jan(169):19-28. doi: 10.1111/j.1742-1241.2010.02604.x.
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.
已经对特发性、遗传性和继发性肺动脉高压（PAH）患者的肺组织、新鲜分离的循环细胞和培养细胞进行了微阵列研究。这些研究提供了关于终末期疾病特征的大量信息，但疾病起源的信息只有在事后才清晰。从这些研究中可以得出的主要结论是，终末期疾病包括大规模但目前定义不明确的炎症反应、为尚未明确的目的诱导血管生成基因、即使在特发性和继发性病例中也抑制BMP途径，以及许多更细微的变化，包括线粒体和肌动蛋白组织变化。此外，通过使用多个基因中的任何一个都可以实现相同的生理终点，因此特定基因通常不如它们所在的途径重要；这条规则的例外情况一定存在于尚未明确的关键节点中。最后，分析方法缺乏一致性使得跨实验比较困难，这可能意味着这些研究中收集的数据有待解读。
