Desmoulière A, Badid C, Bochaton-Piallat M L, Gabbiani G
CNRS-URA 1459, Institut Pasteur de Lyan, France.
Int J Biochem Cell Biol. 1997 Jan;29(1):19-30. doi: 10.1016/s1357-2725(96)00117-3.
Following injury, tissue repair involves inflammation, granulation tissue formation and scar constitution. Granulation tissue develops from the connective tissue surrounding the damaged or missing area and contains mainly small vessels, inflammatory cells, fibroblasts and myofibroblasts. As the wound closes and evolves into a scar, there is a striking decrease in cellularity, including disappearance of typical myofibroblasts. The question arises as to what process is responsible for granulation tissue cell disappearance. Our results (in cutaneous wounds) and results of other laboratories (particularly in lungs and kidney) suggest that apoptosis is the mechanism responsible for the evolution of granulation tissue into a scar. During excessive scarring (hypertrophic scar or fibrosis), it is conceivable that the process of apoptosis cannot take place. After experimental endothelial injury in an artery, accumulation of smooth muscle cells participates in the formation of intimal thickening. Apoptotic features have been observed in cells of intimal thickening and also within human atherosclerotic plaques. In the case of atherosclerosis, apoptosis could be detrimental: since smooth muscle cells participate in plaque stability, apoptosis could lead to weakening and rupture of the plaque. These results underline the fact that both increased cell survival or excessive cell death can be associated with pathological disorders. Specific therapies devised to enhance or decrease the susceptibility of individual cell types to apoptosis development could modify the evolution of a variety of human diseases.
受伤后，组织修复包括炎症反应、肉芽组织形成和瘢痕构成。肉芽组织由受损或缺失区域周围的结缔组织发展而来，主要包含小血管、炎症细胞、成纤维细胞和肌成纤维细胞。随着伤口愈合并演变成瘢痕，细胞数量显著减少，包括典型肌成纤维细胞的消失。于是问题出现了，即肉芽组织细胞消失是由什么过程导致的。我们的研究结果（在皮肤伤口方面）以及其他实验室的结果（特别是在肺和肾方面）表明，细胞凋亡是肉芽组织演变成瘢痕的机制。在过度瘢痕形成（肥厚性瘢痕或纤维化）过程中，可以想象细胞凋亡过程无法发生。在实验性动脉内皮损伤后，平滑肌细胞的积聚参与了内膜增厚的形成。在内膜增厚的细胞以及人类动脉粥样硬化斑块内都观察到了凋亡特征。在动脉粥样硬化的情况下，细胞凋亡可能是有害的：由于平滑肌细胞参与斑块稳定性，细胞凋亡可能导致斑块变弱和破裂。这些结果强调了这样一个事实，即细胞存活增加或细胞过度死亡都可能与病理紊乱相关。设计用于增强或降低个体细胞类型对细胞凋亡易感性的特定疗法可能会改变多种人类疾病的发展进程。
