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铜-肝素吸入疗法修复肺气肿:科学依据。

Copper-Heparin Inhalation Therapy To Repair Emphysema: A Scientific Rationale.

机构信息

Department of Pulmonary Medicine, Canisius-Wilhelmina Hospital, Nijmegen, The Netherlands.

Department of Respiratory Medicine, Maastricht University Medical Center+, Maastricht, The Netherlands.

出版信息

Int J Chron Obstruct Pulmon Dis. 2019 Nov 25;14:2587-2602. doi: 10.2147/COPD.S228411. eCollection 2019.

Abstract

Current pharmacotherapy of chronic obstructive pulmonary disease (COPD) aims at reducing respiratory symptoms and exacerbation frequency. Effective therapies to reduce disease progression, however, are still lacking. Furthermore, COPD medications showed less favorable effects in emphysema than in other COPD phenotypes. Elastin fibers are reduced and disrupted, whereas collagen levels are increased in emphysematous lungs. Protease/antiprotease imbalance has historically been regarded as the sole cause of emphysema. However, it is nowadays appreciated that emphysema may also be provoked by perturbations in the sequential repair steps following elastolysis. Essentiality of fibulin-5 and lysyl oxidase-like 1 in the elastin restoration process is discussed, and it is argued that copper deficiency is a plausible reason for failing elastin repair in emphysema patients. Since copper-dependent lysyl oxidases crosslink elastin as well as collagen fibers, copper supplementation stimulates accumulation of both proteins in the extracellular matrix. Restoration of abnormal elastin fibers in emphysematous lungs is favorable, whereas stimulating pulmonary fibrosis formation by further increasing collagen concentrations and organization is detrimental. Heparin inhibits collagen crosslinking while stimulating elastin repair and might therefore be the ideal companion of copper for emphysema patients. Efficacy and safety considerations may lead to a preference of pulmonary administration of copper-heparin over systemic administration.

摘要

目前慢性阻塞性肺疾病(COPD)的药物治疗旨在减轻呼吸道症状和减少加重频率。然而,仍然缺乏有效的治疗方法来减缓疾病进展。此外,与其他 COPD 表型相比,COPD 药物在肺气肿中的疗效较差。肺气肿的弹性纤维减少和破坏,而胶原蛋白水平增加。蛋白酶/抗蛋白酶失衡一直被认为是肺气肿的唯一原因。然而,如今人们认识到,在弹性蛋白水解后的连续修复步骤中出现的干扰也可能引发肺气肿。弹性蛋白修复过程中纤连蛋白-5 和赖氨酰氧化酶样 1 的必要性正在讨论中,并且有人认为铜缺乏是肺气肿患者弹性蛋白修复失败的一个合理原因。由于铜依赖性赖氨酰氧化酶交联弹性蛋白和胶原蛋白纤维,铜补充刺激细胞外基质中两种蛋白质的积累。在肺气肿的肺部中恢复异常的弹性纤维是有利的,而通过进一步增加胶原蛋白浓度和组织来刺激肺纤维化形成则是有害的。肝素抑制胶原蛋白交联,同时刺激弹性蛋白修复,因此可能是肺气肿患者铜的理想伴侣。疗效和安全性考虑可能导致铜肝素更倾向于肺部给药而不是全身给药。

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