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首页> 外文期刊>Clinical and experimental allergy : >Transforming growth factor-beta1 in asthmatic airway smooth muscle enlargement: is fibroblast growth factor-2 required?
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Transforming growth factor-beta1 in asthmatic airway smooth muscle enlargement: is fibroblast growth factor-2 required?

机译：哮喘气道平滑肌肿大中转化生长因子-β1：是否需要成纤维细胞生长因子-2？

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摘要

Enlargement of airway smooth muscle (ASM) tissue around the bronchi/bronchioles is a histopathological signature of asthmatic airway remodelling and has been suggested to play a critical role in the increased lung resistance and airway hyperresponsiveness seen in asthmatic patients. The pleiotropic cytokine, TGF-beta1, is believed to contribute to several aspects of asthmatic airway remodelling and is known to influence the growth of many cell types. Increased TGF-beta1 expression/signalling and ASM growth have been shown to occur concurrently in animal models of asthma. Abundant studies further substantiate this association by showing that therapeutic strategies that reduce or prevent TGF-beta1 overexpression/signalling lead to a parallel decrease or prevention of ASM enlargement. Finally, recent findings have supported a direct link of causality between TGF-beta1 overexpression/signalling and the overgrowth of ASM tissue. To follow-up on these in vivo studies, many investigators have pursued detailed investigation of ASM in cell culture conditions, assessing the direct role of TGF-beta1 on cellular proliferation and/or hypertrophy. Inconsistencies among the in vitro studies suggest that the effect of TGF-beta1 on ASM cell proliferation/hypertrophy is contextual. A hypothesis focusing on fibroblast growth factor-2 is presented at the end of this review, which could potentially reconcile the apparent discrepancy between the conflicting in vitro findings with the consistent in vivo finding that TGF-beta1 is required for ASM enlargement in asthma.
机译：支气管/细支气管周围的气道平滑肌（ASM）组织增大是哮喘气道重塑的组织病理学特征，并且已被认为在哮喘患者中看到的肺阻力增加和气道高反应性中起关键作用。多效性细胞因子TGF-β1被认为有助于哮喘气道重塑的多个方面，并且已知会影响许多细胞类型的生长。在哮喘动物模型中，TGF-beta1表达/信号增强和ASM增长同时发生。大量的研究通过证明减少或防止TGF-beta1过表达/信号转导的治疗策略可同时减少或防止ASM增大，进一步证实了这种联系。最后，最新发现支持TGF-beta1过表达/信号传递与ASM组织过度生长之间的因果关系。为了对这些体内研究进行跟踪，许多研究人员对细胞培养条件下的ASM进行了详细研究，评估了TGF-β1对细胞增殖和/或肥大的直接作用。体外研究之间的矛盾表明，TGF-β1对ASM细胞增殖/肥大的影响是背景性的。在这篇综述的最后提出了一个针对成纤维细胞生长因子2的假说，该假说可以潜在地解决相互矛盾的体外发现与哮喘ASM扩大需要TGF-β1的一致体内发现之间的明显差异。

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