2010年Science杂志十大科学突破之一就是有关iPS新型培养方法的，这种诱导多功能干细胞技术由于绕开了胚胎干细胞研究面临的伦理和法律等障碍，因此在医疗领域的应用前景非常广阔。但是iPS细胞的应用由于其潜在致癌性和效率低，不利其未来的临床应用，科学家们如果要想借助干细胞疗法治疗疾病仍然需要更多的深入研究。

在最新研究中，研究人员利用一种酶的抑制剂：ROCK（Rho-associated coiled-coil forming kinase/Rho结合酶）抑制剂代替动物成分，刺激干细胞重新编程，从而获得iPS细胞。

一般的iPS细胞重编程过程需要依赖于一些动物成分，比如动物血清和活细胞，但是如果应用到临床，就会导致病人感染动物疾病，而且iPS诱导过程也需要用到病毒因子，这样引入的多余成分可能会造成病人移植干细胞后患上癌症。

研究人员利用ROCK抑制剂诱导iPS细胞，并且利用获得的细胞培养间叶系干细胞，移植到因血管受到破坏而导致肢体功能受损的小鼠身上，结果发现间叶系干细胞可形成新的血管，改善血液循环，这对于各种心血管疾病的治疗来说无疑是一个福音。而且利用这种方法还可以培养多种人体组织细胞，包括心脏、脑、血管、肝脏等，提供了无限量的人类细胞来源，让医生更容易分析疾病的演变过程，以及直接在细胞培养皿上利用这些细胞检测药物反应。

原文摘要：

A Human iPSC Model of Hutchinson Gilford Progeria Reveals Vascular Smooth Muscle and Mesenchymal Stem Cell Defects.

The segmental premature aging disease Hutchinson-Gilford Progeria syndrome (HGPS) is caused by a truncated and farnesylated form of Lamin A called progerin. HGPS affects mesenchymal lineages, including the skeletal system, dermis, and vascular smooth muscle (VSMC). To understand the underlying molecular pathology of HGPS, we derived induced pluripotent stem cells (iPSCs) from HGPS dermal fibroblasts. The iPSCs were differentiated into neural progenitors, endothelial cells, fibroblasts, VSMCs, and mesenchymal stem cells (MSCs). Progerin levels were highest in MSCs, VSMCs, and fibroblasts, in that order, with these lineages displaying increased DNA damage, nuclear abnormalities, and HGPS-VSMC accumulating numerous calponin-staining inclusion bodies. Both HGPS-MSC and -VSMC viability was compromised by stress and hypoxia in vitro and in vivo (MSC). Because MSCs reside in low oxygen niches in vivo, we propose that, in HGPS, this causes additional depletion of the MSC pool responsible for replacing differentiated cells lost to progerin toxicity.