摘要
肌成纤维细胞活化是组织纤维化发病机制中的关键过程，占所有死亡的45％。没有有效的治疗方法可用于治疗纤维化疾病。我们将我们的小型评论集中在最近的数据上，这些数据显示已知为强效Na +，K + -ATP酶抑制剂的强心类固醇（CTS）以细胞类型特异性方式影响肌成纤维细胞分化。在培养的人肺成纤维细胞（HLF），上皮细胞和癌相关成纤维细胞中，CTS阻断由促纤维化细胞因子TGF-β触发的肌成纤维细胞分化。相反，在不存在TGF-β的情况下，CTS增强了培养的心脏成纤维细胞的肌成纤维细胞分化。 CTS在肌成纤维细胞分化中的细胞类型特异性作用与体内研究中获得的数据一致。因此，通过渗透微型泵输注哇巴因减弱了经博来霉素处理的小鼠中肺纤维化的发展，而marinobufagenin刺激了具有实验性肾损伤的大鼠的肾和心脏纤维化。在TGF-β处理的HLF中，哇巴因对肌成纤维细胞分化的抑制是由[Na +] i / [K +] i比率的升高介导的，并且伴随着环加氧酶COX-2的上调和TGF-β受体TGFBR2的下调。通过抑制Na + / Ca 2+交换来消除COX-2的增强表达，表明[Ca 2+] i介导的信号传导的关键作用。在几种类型的CTS处理细胞中记录的[Na +] i，[K +] iindependent信号传导对组织纤维化的相对影响是什么？在哇巴因和marinobufagenin存在下，Na +，K +-ATPaseα1亚基的不同构象转变是否有助于它们明显参与肌成纤维细胞分化？应该进行另外的实验来回答这些问题并开发用于治疗纤维化相关病症的新型药理学方法。
关键词: Na +，K + -ATP酶，心脏类固醇，纤维化，肌成纤维细胞，环加氧酶，TGF-β受体，COX-2，细胞内Na +和K +。
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