Zhou Limei, Hershenson Marc B
Department of Pediatrics, University of Chicago, Chicago, IL 48109-0688, USA.
Respir Physiol Neurobiol. 2003 Sep 16;137(2-3):295-308. doi: 10.1016/s1569-9048(03)00154-x.
Increased airway smooth muscle mass has been demonstrated in patients with asthma, bronchopulmonary dysplasia and most recently, cystic fibrosis. These observations emphasize the need for further knowledge of the events involved in airway smooth muscle mitogenesis and hypertrophy. Workers in the field have developed cell culture systems involving tracheal and bronchial myocytes from different species. An emergent body of literature indicates that mutual signal transduction pathways control airway smooth muscle cell cycle entry across species lines. This article reviews what is known about mitogen-activated signal transduction in airway myocytes. The extracellular signal regulated kinase (ERK) and phosphatidylinositol 3-kinase (PI 3-kinase) pathways appear to be key positive regulators of airway smooth muscle mitogenesis; recent studies have also demonstrated specific roles for reactive oxygen and the JAK/STAT pathway. It is also possible that growth factor stimulation of airway smooth muscle concurrently elicits signaling through negative regulatory intermediates such as p38 mitogen-activated protein (MAP) kinase and protein kinase C (PKC) delta, conceivably as a defense against extreme growth.
哮喘、支气管肺发育不良以及最近发现的囊性纤维化患者体内，气道平滑肌质量均有所增加。这些观察结果强调了进一步了解气道平滑肌有丝分裂和肥大相关事件的必要性。该领域的研究人员已开发出涉及不同物种气管和支气管肌细胞的细胞培养系统。大量新出现的文献表明，相互的信号转导途径跨物种控制气道平滑肌细胞周期进入。本文综述了关于气道肌细胞有丝分裂原激活信号转导的已知情况。细胞外信号调节激酶（ERK）和磷脂酰肌醇3激酶（PI 3激酶）途径似乎是气道平滑肌有丝分裂的关键正向调节因子；最近的研究还证明了活性氧和JAK/STAT途径的特定作用。气道平滑肌生长因子刺激也可能同时通过负调节中间体如p38丝裂原活化蛋白（MAP）激酶和蛋白激酶C（PKC）δ引发信号传导，这可以想象为对过度生长的一种防御机制。
