Paradigm Shifts in Atherosclerotic Renovascular Disease: Where Are We Now?
Paradigm Shifts in Atherosclerotic Renovascular Disease: Where Are We Now?
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DOI：
10.1681/asn.2014121274
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发表时间：
2015-04
期刊：
影响因子：
--
通讯作者：
S. Textor;L. Lerman
中科院分区：
文献类型：
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作者：
S. Textor;L. Lerman
最近的临床试验和实验研究结果表明，尽管动脉粥样硬化性肾血管疾病可加速狭窄后肾脏的全身性高血压和组织损伤，但仅恢复血管通畅不足以恢复大多数受试者的肾功能。动脉粥样硬化性肾血管疾病的肾损伤反映了血管稀薄、氧化应激损伤和最终产生纤维化的炎症细胞因子募集之间复杂的相互作用。简单恢复血流的经典范例正在转变为针对线粒体和细胞功能的治疗，以允许血管、肾小球和小管结构的再生，足以恢复或至少稳定肾功能。这些进展为肾脏组织的修复和再生提供了令人兴奋的可能性，这可能会限制动脉粥样硬化性肾血管疾病中CKD的进展，并可能适用于其他炎症损伤是主要共同途径的疾病。
Results of recent clinical trials and experimental studies indicate that whereas atherosclerotic renovascular disease can accelerate both systemic hypertension and tissue injury in the poststenotic kidney, restoring vessel patency alone is insufficient to recover kidney function for most subjects. Kidney injury in atherosclerotic renovascular disease reflects complex interactions among vascular rarefication, oxidative stress injury, and recruitment of inflammatory cellular elements that ultimately produce fibrosis. Classic paradigms for simply restoring blood flow are shifting to implementation of therapy targeting mitochondria and cell-based functions to allow regeneration of vascular, glomerular, and tubular structures sufficient to recover, or at least stabilize, renal function. These developments offer exciting possibilities of repair and regeneration of kidney tissue that may limit progressive CKD in atherosclerotic renovascular disease and may apply to other conditions in which inflammatory injury is a major common pathway.