Complement-Mediated Glomerular Diseases: A Tale of 3 Pathways.
Complement-Mediated Glomerular Diseases: A Tale of 3 Pathways.
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DOI：
10.1016/j.ekir.2016.06.005
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发表时间：
2016-09
影响因子：
6
通讯作者：
Appel GB
中科院分区：
文献类型：
--
作者：
Bomback AS;Markowitz GS;Appel GB
人们对补体在肾小球疾病发病机制中的作用重新产生了兴趣，这提高了我们对其基本的、潜在的生理学的理解。所有三种补体途径--经典途径、凝集素途径和替代途径--都与罕见的肾小球病变(如致密沉淀性疾病)和常见的(如IgA肾病)有关。在这里，我们回顾了这些通路的基本功能，并重点强调了激活如何导致肾小球损伤。最后，我们将探讨补体靶向治疗作为肾小球疾病的疾病特异性干预的前景。
A renewed interest in the role of complement in the pathogenesis of glomerular diseases has improved our understanding of their basic, underlying physiology. All 3 complement pathways—classical, lectin, and alternative—have been implicated in glomerular lesions both rare (e.g., dense deposit disease) and common (e.g., IgA nephropathy). Here we review the basic function of these pathways and highlight, with a disease-specific focus, how activation can lead to glomerular injury. We end by exploring the promise of complement-targeted therapies as disease-specific interventions for glomerular diseases.