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内皮细胞糖萼在脓毒症诱导的急性肾损伤中的作用

Role of the endothelial cell glycocalyx in sepsis-induced acute kidney injury.

作者信息

Wang Yixun, Zhang Zhaohui, Qu Xingguang, Zhou Gaosheng

机构信息

The First College of Clinical Medical Science, China Three Gorges University, Yichang, China.

Department of Critical Care Medicine, Yichang Central People's Hospital, Yichang, China.

出版信息

Front Med (Lausanne). 2025 Apr 4;12:1535673. doi: 10.3389/fmed.2025.1535673. eCollection 2025.

Abstract

Sepsis-induced acute kidney injury (S-AKI) is a common complication of sepsis. It occurs at high incidence and is associated with a high level of mortality in the intensive care unit (ICU). The pathophysiologic mechanisms underlying S-AKI are complex, and include renal vascular endothelial cell dysfunction. The endothelial glycocalyx (EG) is a polysaccharide/protein complex located on the cell membrane at the luminal surface of vascular endothelial cells that has anti-inflammatory, anti-thrombotic, and endothelial protective effects. Recent studies have shown that glycocalyx damage plays a causal role in S-AKI progression. In this review, we first describe the structure, location, and basic function of the EG. Second, we analyze the underlying mechanisms of EG degradation in sepsis and S-AKI. Finally, we provide a summary of the potential therapeutic strategies that target the EG.

摘要

脓毒症诱导的急性肾损伤(S-AKI)是脓毒症常见的并发症。其发病率高,与重症监护病房(ICU)的高死亡率相关。S-AKI潜在的病理生理机制复杂,包括肾血管内皮细胞功能障碍。内皮糖萼(EG)是位于血管内皮细胞管腔表面细胞膜上的多糖/蛋白质复合物,具有抗炎、抗血栓形成和内皮保护作用。最近的研究表明,糖萼损伤在S-AKI进展中起因果作用。在本综述中,我们首先描述EG的结构、位置和基本功能。其次,我们分析脓毒症和S-AKI中EG降解的潜在机制。最后,我们总结了针对EG的潜在治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78df/12006053/f43317755e06/fmed-12-1535673-g001.jpg

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