Pathophysiological role of chymase in complications of metabolic syndrome

糜酶将血管紧张素II、转化生长因子-β和基质金属蛋白酶-9的前体转化为它们的活性形式。在糖尿病动物模型中，凝乳酶通过促进凝乳酶形成和血管紧张素Ⅱ诱导胰腺组织紊乱。在腹主动脉瘤样病变(AAA)动物模型中，凝乳酶抑制剂抑制基质金属蛋白酶-9的激活，导致AAA进展的减缓。在非酒精性脂肪性肝炎的动物模型中，抑制糜酶可以有效地预防肝脏的脂肪变性和纤维化。这些结果表明，糜酶在代谢综合征的并发症中起着关键作用。

Chymase converts precursors of angiotensin (Ang) II, Transforming growth factor (TGF)-β and matrix metalloproteinase (MMP)-9 to their active forms. In a diabetic animal model, chymase induced pancreatic disorganization by augmentation of chymase-forming Ang II. In an animal model with abdominal aneurysmal aorta (AAA), the inhibition of MMP-9 activation by chymase inhibitor resulted in attenuation of the AAA progression. Steatosis and fiblosis in liver were strongly prevented by chymase inhibition in an animal model with nonalcoholic steatohepatitis. These results demonstrated that chymase plays a crucial role in complications of metabolic syndrome.