Department of Physiology and Biophysics, Center for Excellence in Cardiovascular-Renal Research, and University of Mississippi Medical Center, Jackson, Mississippi 39216-4505, USA.
Am J Physiol Regul Integr Comp Physiol. 2011 Apr;300(4):R783-90. doi: 10.1152/ajpregu.00657.2010. Epub 2011 Feb 9.
Emerging evidence supports the pivotal role of renal microvascular disease as a determinant of tubulo-interstitial and glomerular fibrosis in chronic kidney disease. An intact microcirculation is vital to restore blood flow to the injured tissues, which is a crucial step to achieve a successful repair response. The purpose of this review is to discuss the impact and mechanisms of the functional and structural changes of the renal microvascular network, as well as the role of these changes in the progression and irreversibility of renal injury. Damage of the renal microcirculation and deterioration of the angiogenic response may constitute early steps in the complex pathways involved in progressive renal injury. There is limited but provocative evidence that stimulation of vascular proliferation and repair may stabilize renal function and slow the progression of renal disease. The feasibility of novel potential therapeutic interventions for stabilizing the renal microvasculature is also discussed. Targeted interventions to enhance endogenous renoprotective mechanisms focused on the microcirculation, such as cell-based therapy or the use of angiogenic cytokines have shown promising results in some experimental and clinical settings.
新出现的证据支持肾微血管疾病作为慢性肾脏病肾小管间质和肾小球纤维化的决定因素的关键作用。完整的微循环对于恢复受损组织的血流至关重要，这是实现成功修复反应的关键步骤。本文的目的是讨论肾微血管网络的功能和结构变化的影响和机制，以及这些变化在肾损伤的进展和不可逆转中的作用。肾微循环的损伤和血管生成反应的恶化可能构成参与进行性肾损伤的复杂途径中的早期步骤。虽然证据有限，但有一些有启发性的证据表明，刺激血管增殖和修复可能稳定肾功能并减缓肾脏病的进展。还讨论了稳定肾微血管的新型潜在治疗干预措施的可行性。针对增强内源性肾保护机制的靶向干预措施，如基于细胞的治疗或使用血管生成细胞因子，在一些实验和临床环境中显示出有希望的结果。
