Fogo A B
Department of Pathology, Vanderbilt University Medical Center, Nashville, Tenn., USA.
Exp Nephrol. 1999 Mar-Apr;7(2):147-59. doi: 10.1159/000020595.
Progressive deterioration of the kidney is common to many renal diseases. The structural injuries which lead to this progressive loss of function consist of focal segmental glomerulosclerosis and tubulointerstitial fibrosis and atrophy. These processes were previously thought to be inexorable, regardless of the primary disease. However, recent observations point to the possibility of reversal of sclerosis. Mesangial matrix accumulation is the cornerstone of glomerulosclerosis and results when matrix synthesis exceeds matrix degradation. The renin-angiotensin system appears to be one central component of this process, with links to numerous mechanisms which promote matrix accumulation. Most recently, direct induction of plasminogen activator inhibitor-1 by angiotensin has been recognized. Plasminogen activator inhibitor-1 not only promotes thrombosis, but also inhibits matrix degradation. The various mechanisms which modulate mesangial matrix accumulation and their potential reversibility are reviewed.
肾脏功能的进行性恶化在许多肾脏疾病中都很常见。导致这种功能逐渐丧失的结构损伤包括局灶节段性肾小球硬化以及肾小管间质纤维化和萎缩。这些过程以前被认为是不可阻挡的，无论原发性疾病是什么。然而，最近的观察结果表明硬化有可能逆转。系膜基质积聚是肾小球硬化的基石，当基质合成超过基质降解时就会出现这种情况。肾素 - 血管紧张素系统似乎是这一过程的一个核心组成部分，与许多促进基质积聚的机制相关。最近，已认识到血管紧张素可直接诱导纤溶酶原激活物抑制剂 -1。纤溶酶原激活物抑制剂 -1不仅促进血栓形成，还抑制基质降解。本文综述了调节系膜基质积聚的各种机制及其潜在的可逆性。
