肺纖維化至目前為止仍是臨床上一棘手問題。它可能起始於肺部發炎反應, 進一步透過氧游離基、細胞素、生長因子的作用造成肺組織內各種細胞外基質的金屬蛋白與金屬蛋白抑制劑的分佈失衡，造成過量的膠原蛋白堆積在肺組織，以致於肺順應性改變、肺容積明顯變小，呼吸困難，呼吸衰竭等臨床症狀。本評論先對抗癌用葯Bleomycin 引起肺部組織的纖維化作一簡介，然後再環繞在胞外基質蛋白表現與肺纖維化發生的關係作一簡要的描述。

Currently, lung fibrosis is still a difficult clinical problem. It caninitially occur due to lung inflammation then be further exacerbated by the reaction of oxygenradicals, cytokines, and growth factors to induce an imbalance between matrix extracellularmetalloproteinases (MMPs) and their inhibitors, tissue inhibitors of matrix metalloproteinases(TIMPs) . This causes excess collagen proteins to accumulate in lung tissues, inducing clinicalsymptoms such as lung compliance changes, lung volume decreases, dyspnea, and respiratory failure.In this comment we focus on the induction of lung fibrosis by bleomycin, an anticancer drug.Furthermore, we correlate lung fibrosis with MMP expressions.