Role of Chitinase in the Development and Advance in Atherosclerosis

在巨噬细胞中过表达或抑制几丁质酶的实验表明，几丁质酶通过PPARγ和LXRα途径增加CD36、ABCA1和Abcg1的表达，促进胆固醇摄取和依赖于Apo-AI的胆固醇外流，并通过抑制AP-1的转录活性来减少炎性细胞因子MCP-1和肿瘤坏死因子α的表达。给予几丁质酶抑制剂可增加载脂蛋白E基因敲除小鼠的动脉粥样硬化病变。这些数据表明，几丁质酶具有抗动脉粥样硬化的作用。

Experiments overexpressing or inhibiting chitinase in cultured macrophages revealed that chitinase increased CD36, ABCA1, and ABCG1 expression via PPARγ and LXRα pathway, promoted cholesterol uptake and Apo-AI dependent cholesterol efflux, and decreased inflammatory cytokines MCP-1 and TNFα expression by suppressing AP-1 transcriptional activity. Administration of chitinase inhibitor increased atherosclerotic lesion in ApoE knockout mice. These data suggest that chitinase has anti-atherosclerotic effects.