The Department of Physiology and Biophysics, Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Compr Physiol. 2013 Apr;3(2):817-31. doi: 10.1002/cphy.c120012.
An intact microcirculation is vital for diffusion of oxygen and nutrients and for removal of toxins of every organ and system in the human body. The functional and/or anatomical loss of microvessels is known as rarefaction, which can compromise the normal organ function and have been suggested as a possible starting point of several diseases. The purpose of this overview is to discuss the potential underlying mechanisms leading to renal microvascular rarefaction, and the potential consequences on renal function and on the progression of renal damage. Although the kidney is a special organ that receives much more blood than its metabolic needs, experimental and clinical evidence indicates that renal microvascular rarefaction is associated to prevalent cardiovascular diseases such as diabetes, hypertension, and atherosclerosis, either as cause or consequence. On the other hand, emerging experimental evidence using progenitor cells or angiogenic cytokines supports the feasibility of therapeutic interventions capable of modifying the progressive nature of microvascular rarefaction in the kidney. This overview will also attempt to discuss the potential renoprotective mechanisms of the therapeutic targeting of the renal microcirculation.
完整的微循环对于人体每个器官和系统的氧气和营养物质的扩散以及毒素的清除至关重要。微血管的功能和/或解剖学丧失被称为稀疏,这可能会损害正常的器官功能,并被认为是几种疾病的可能起点。本篇综述的目的是讨论导致肾微血管稀疏的潜在潜在机制,以及对肾功能和肾脏损伤进展的潜在影响。尽管肾脏是一个特殊的器官,其接受的血液比其代谢需求多得多,但实验和临床证据表明,肾微血管稀疏与常见的心血管疾病(如糖尿病、高血压和动脉粥样硬化)有关,无论是作为原因还是结果。另一方面,使用祖细胞或血管生成细胞因子的新兴实验证据支持了治疗干预的可行性,这些干预措施能够改变肾脏微血管稀疏的进行性。本篇综述还将尝试讨论治疗性靶向肾脏微循环的潜在肾脏保护机制。