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维生素 K 缺乏与肺弹力纤维退行性疾病的弹性溶解学说。

Vitamin K deficit and elastolysis theory in pulmonary elasto-degenerative diseases.

机构信息

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

R&D Group VitaK, Maastricht University, Maastricht, The Netherlands.

出版信息

Med Hypotheses. 2017 Oct;108:38-41. doi: 10.1016/j.mehy.2017.07.029. Epub 2017 Jul 21.

Abstract

Elastin is a unique protein providing deformability and resilience to dynamic tissues, such as arteries and lungs. It is an absolute basic requirement for circulation and respiration. Elastin can be degraded by elastases and has a high calcium affinity. Elastin calcification and elastin degradation are two pathological processes that impair elastin's functioning. Furthermore, elastin degradation can be associated to elastin calcification. Matrix Gla Protein (MGP) is probably the most potent natural inhibitor of elastin calcification and requires vitamin K for its activation. Measuring circulating levels of inactive MGP (dp-ucMGP) is a frequently used method to assess vitamin K status. Dp-ucMGP reflects the burden of vitamin K-dependent proteins that have not been activated by vitamin K and could therefore best be regarded as a biomarker of a vitamin K deficit. Dp-ucMGP levels decrease after vitamin K supplementation. Since the amino acids desmosine and isodesmosine (DES) are unique to crosslinked elastin fibers, systemic elastin degradation can be assessed with the plasma DES assay. Recently, we discovered a strong correlation between plasma dp-ucMGP and plasma DES levels in both patients with chronic obstructive pulmonary disease (COPD) and controls. The 'Vitamin K deficit and elastolysis theory' posits that elastin degradation causes a rise in the vitamin K deficit and implies that vitamin K supplementation could be preventing elastin degradation. If this hypothesis holds true and is universally found in every state and condition, it will have an unprecedented impact on the management of every single pulmonary disease characterized by accelerated elastin degradation, such as alpha-1 antitrypsin deficiency, bronchiectasis, COPD and cystic fibrosis. Theoretically, a plasma dp-ucMGP concentration of zero would be associated with a near-complete standstill of elastin degradation and disease progression in patients with any of these debilitating conditions.

摘要

弹性蛋白是一种为动脉和肺等动态组织提供可变形性和弹性的独特蛋白质。它是血液循环和呼吸的绝对基本要求。弹性蛋白可被弹性蛋白酶降解,并且具有高钙亲和力。弹性蛋白钙化和弹性蛋白降解是两种损害弹性蛋白功能的病理过程。此外,弹性蛋白降解可能与弹性蛋白钙化有关。基质 Gla 蛋白(MGP)可能是最有效的天然弹性蛋白钙化抑制剂,并且其激活需要维生素 K。测量无活性 MGP(dp-ucMGP)的循环水平是评估维生素 K 状态的常用方法。dp-ucMGP 反映了未被维生素 K 激活的维生素 K 依赖性蛋白质的负担,因此可以最好地被视为维生素 K 缺乏的生物标志物。补充维生素 K 后 dp-ucMGP 水平下降。由于去甲氧基素和异去甲氧基素(DES)是交联弹性纤维所特有的氨基酸,因此可以通过血浆 DES 测定来评估系统性弹性蛋白降解。最近,我们发现慢性阻塞性肺疾病(COPD)患者和对照组的血浆 dp-ucMGP 和血浆 DES 水平之间存在很强的相关性。“维生素 K 缺乏和弹性蛋白降解理论”认为弹性蛋白降解会导致维生素 K 缺乏增加,并暗示维生素 K 补充可能会阻止弹性蛋白降解。如果这一假设成立并且在每种状态和条件下都普遍存在,它将对所有以加速弹性蛋白降解为特征的肺部疾病的管理产生前所未有的影响,如α-1 抗胰蛋白酶缺乏症、支气管扩张症、COPD 和囊性纤维化。从理论上讲,这些使人衰弱的条件中的任何一种患者的血浆 dp-ucMGP 浓度为零将与弹性蛋白降解和疾病进展的近乎完全停滞相关。

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