Camici Marcello, Carpi Angelo, Cini Giuseppe, Galetta Fabio, Abraham Nader
Department of Internal Medicine, Pisa University, Pisa, Italy.
Front Biosci (Schol Ed). 2011 Jun 1;3(3):995-1006. doi: 10.2741/204.
We review podocyte molecular structure and function, consider the underlying mechanisms related to podocyte dysfunction and propose that podocyte dysfunction be considered in the evaluation and management of age-associated glomerulosclerosis. With aging, progressive sympathetic activation, increased intrarenal renin-angiotensin system (RAS) activity, endothelin system and oxidative stress and reduced nitric oxide (NO)-availability can damage podocytes. Apoptosis and proliferation are the principal podocyte changes following injury with the latter leading to sclerosis and loss of nephrons. Podocyte loss can be evaluated by either determining their average number in biopsed glomeruli or by estimating podocyte number or their associated molecules in urine sediment. Podocyturia may be considered a marker of active glomerular disease. Preliminary data suggest that antiadrenergic drugs, angiotensin converting enzyme (ACE) inhibitors, RAS blocking drugs, endothelin system inhibitors and reduced oxidative stress can protect podocytes. Thus podocytes appear to play an important role in the pathogenesis, evaluation and therapy of age related glomerulosclerosis.
我们回顾了足细胞的分子结构和功能，探讨了与足细胞功能障碍相关的潜在机制，并建议在评估和管理年龄相关性肾小球硬化时考虑足细胞功能障碍。随着年龄增长，渐进性交感神经激活、肾内肾素-血管紧张素系统（RAS）活性增加、内皮素系统和氧化应激以及一氧化氮（NO）可用性降低会损害足细胞。凋亡和增殖是足细胞损伤后的主要变化，后者导致硬化和肾单位丧失。足细胞丢失可通过确定活检肾小球中它们的平均数量或通过估计尿沉渣中足细胞数量或其相关分子来评估。足细胞尿可被视为活动性肾小球疾病的标志物。初步数据表明，抗肾上腺素能药物、血管紧张素转换酶（ACE）抑制剂、RAS阻断药物、内皮素系统抑制剂和氧化应激减轻可保护足细胞。因此，足细胞似乎在年龄相关性肾小球硬化的发病机制、评估和治疗中起重要作用。
