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心脏成纤维细胞在心脏重构中起重要作用。在各种促纤维化因素(如前炎症因子、缺氧-复氧、压力超负荷、衰老)刺激下,心脏成纤维细胞增殖、迁移、激活,导致细胞基质成分的积聚、心脏肥厚和僵硬。过氧化物酶增殖体激活受体γ(PPAR-γ)的配体,特别是噻唑烷二酮类胰岛素增敏药,在病理条件下可调节心脏成纤维细胞的功能以及心脏重构的发展,然而未发现噻唑烷二酮类胰岛素增敏药对心脏衰竭的有益作用。噻唑烷二酮类胰岛素增敏药调节心脏成纤维细胞功能和心脏重构的确切信号通路未完全阐明,现有证据提示涉及氧化应激及相关信号途径。此外,PPAR-γ和植物凝集素样氧化型低密度脂蛋白受体-1(LOX-1)在其中起重要作用。
Cardiac fibroblasts play an important role in cardiac remodeling. Cardiac fibroblasts proliferate, migrate, and activate, resulting in accumulation of cellular matrix components, cardiac hypertrophy and stiffness under various pro-fibrotic factors (eg, proinflammatory cytokines, hypoxia-reoxygenation, stress overload, and aging). Ligands of peroxisome proliferator activated receptor γ (PPAR-γ), in particular thiazolidinedione-sensitizing insulin, regulate the function of cardiac fibroblasts and the development of cardiac remodeling under pathological conditions, However, no beneficial effect of thiazolidinedione-based insulin sensitizers on heart failure was found. The exact signaling pathways by which thiazolidinediones insulin sensitizers regulate cardiac fibroblast function and cardiac remodeling are not fully elucidated. There is evidence that oxidative stress and related signaling pathways are involved. In addition, PPAR-γ and Lectin-Like Oxidized Low Density Lipoprotein Receptor-1 (LOX-1) play an important role.