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心肌纤维化 (MF)是高血压左室重构的主要表现之一 ,TGF β1和AngII是这一过程中的重要生物活性因子 ,AngII通过血管紧张素II 1型 (AT1)受体对TGF β1合成和释放的刺激 ,增加TGF β1的表达和促进纤维的发生 ;TGF β1也上调I型、III型胶原合成并抑制胶原酶的释放 ;两者相互作用 ,共同促进MF的发生。多种药物可对TGF β1的表达产生抑制 ,AT1受体拮抗剂、血管紧张素转换酶抑制剂和TGF β拮抗剂在降低TGF β1表达和减轻MF方面显示良好作用。
Myocardial fibrosis (MF) is one of the major manifestations of hypertension-induced left ventricular remodeling. TGF-β1 and AngII are important bioactive factors in this process. AngII inhibits the expression of TGF-β1 through angiotensin II type 1 (AT1) Synthesis and release of stimulation, increase the expression of TGF β1 and promote the occurrence of fiber; TGF β1 also increased type I, type III collagen synthesis and inhibition of collagenase release; interaction between the two to jointly promote the occurrence of MF. A variety of drugs can inhibit the expression of TGFβ1, AT1 receptor antagonists, angiotensin converting enzyme inhibitors and TGFβ antagonists in reducing TGFβ1 expression and reduce the MF showed a good effect.