Centro de Pesquisas Gonçalo Moniz, Fundação Oswaldo Cruz, Salvador, Brazil.
J Infect Dis. 2010 Aug 15;202(3):416-26. doi: 10.1086/653481.
Chronic chagasic cardiomyopathy is a leading cause of heart failure in Latin American countries. About 30% of Trypanosoma cruzi-infected individuals develop this severe symptomatic form of the disease, characterized by intense inflammatory response accompanied by fibrosis in the heart. We performed an extensive microarray analysis of hearts from a mouse model of this disease and identified significant alterations in expression of approximately 12% of the sampled genes. Extensive up-regulations were associated with immune-inflammatory responses (chemokines, adhesion molecules, cathepsins, and major histocompatibility complex molecules) and fibrosis (extracellular matrix components, lysyl oxidase, and tissue inhibitor of metalloproteinase 1). Our results indicate potentially relevant factors involved in the pathogenesis of the disease that may provide new therapeutic targets in chronic Chagas disease.
慢性恰加斯心肌病是拉丁美洲国家心力衰竭的主要原因。约 30%的克氏锥虫感染个体发展为这种严重的疾病症状形式，其特征是心脏中强烈的炎症反应伴有纤维化。我们对这种疾病的小鼠模型的心脏进行了广泛的微阵列分析，发现大约 12%的取样基因的表达发生了显著改变。广泛的上调与免疫炎症反应（趋化因子、粘附分子、组织蛋白酶和主要组织相容性复合体分子）和纤维化（细胞外基质成分、赖氨酰氧化酶和金属蛋白酶组织抑制剂 1）有关。我们的研究结果表明，与疾病发病机制相关的潜在相关因素可能为慢性恰加斯病提供新的治疗靶点。
