TGF-beta/Smad signalling in macrophage-mediated renal fibrosis.

巨噬细胞介导的肾纤维化中的 TGF-β/Smad 信号传导。

• 批准号: nhmrc : GNT1122073
• 负责人: A/Pr David Nikolic-Paterson
• 金额: $ 68.37万
• 依托单位: Monash University
• 依托单位国家: 澳大利亚
• 项目类别: Project Grants
• 财政年份: 2017
• 资助国家: 澳大利亚
• 起止时间: 2017-01-01 至 无数据
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/tgf-betasmad-signalling-renal-fibrosis/1347245
• 关键词: TGF; beta; Smad; signalling; macrophage

Scarring of organs such as the kidney, lung or liver is a common mechanism leading to organ failure and death. We postulate that a type of white blood cell (the macrophage) can transition into the cell type (the fibroblast) responsible for making the excess collagen that leads to this scarring. If proven, this will be a major advance in our understanding of organ fibrosis and may identify new therapeutic approaches to currently intractable diseases.

肾、肺或肝脏等器官的疤痕是导致器官衰竭和死亡的常见机制。我们推测，一种类型的白细胞(巨噬细胞)可以转变为负责制造过量胶原的细胞类型(成纤维细胞)，从而导致瘢痕形成。如果得到证实，这将是我们对器官纤维化理解的重大进步，并可能为目前难以治愈的疾病找到新的治疗方法。