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移植患者的胆固醇外流。

Cholesterol efflux in the transplant patient.

机构信息

Washington University School of Medicine, Saint Louis, Missouri, USA.

出版信息

Curr Opin Endocrinol Diabetes Obes. 2018 Apr;25(2):143-146. doi: 10.1097/MED.0000000000000390.

Abstract

PURPOSE OF REVIEW

Cholesterol metabolism is increasingly recognized in inflammatory diseases including transplantation. This review discusses the mechanistic underpinnings that tie macrophage cholesterol efflux capacity (CEC) of high-density lipoprotein (HDL) to chronic rejection in transplanted patients.

RECENT FINDINGS

Animal studies suggest that administration of apolipoprotein A-I, the main protein constituent of HDL, can prevent transplant arteriosclerosis. apoA-I administration increases CEC of HDL. In patients with cardiac allograft vasculopathy (CAV), decreased CEC has been associated with poorer survival. In addition, reduced CEC in recipients, pretransplant, has been associated with the development of CAV and renal allograft survival.

SUMMARY

These recent findings raise the hypothesis that increasing cholesterol efflux may prevent chronic rejection and improve allograft survival after transplant. Reconstituted HDL significantly increases CEC and is currently in clinical development for traditional atherosclerosis. Clinical trials of reconstituted HDL administration in transplantation should be performed.

摘要

目的综述

胆固醇代谢在包括移植在内的炎症性疾病中越来越受到重视。本综述讨论了将巨噬细胞胆固醇流出能力(CEC)与移植患者慢性排斥反应联系起来的机制基础。

最近的发现

动物研究表明,载脂蛋白 A-I(HDL 的主要蛋白成分)的给药可以预防移植性动脉硬化。apoA-I 给药可增加 HDL 的 CEC。在心脏同种异体移植血管病(CAV)患者中,CEC 降低与生存率降低相关。此外,移植前受者 CEC 降低与 CAV 的发展和肾移植存活相关。

总结

这些最近的发现提出了这样一种假设,即增加胆固醇流出可能预防慢性排斥反应并改善移植后的同种异体移植物存活。重组 HDL 可显著增加 CEC,目前正在开发用于传统动脉粥样硬化。应进行移植中重组 HDL 给药的临床试验。

相似文献

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Cholesterol efflux in the transplant patient.移植患者的胆固醇外流。
Curr Opin Endocrinol Diabetes Obes. 2018 Apr;25(2):143-146. doi: 10.1097/MED.0000000000000390.

本文引用的文献

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Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease.卡那奴单抗治疗动脉粥样硬化疾病的抗炎疗法。
N Engl J Med. 2017 Sep 21;377(12):1119-1131. doi: 10.1056/NEJMoa1707914. Epub 2017 Aug 27.

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