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炎症、代谢和凝血对周围动脉疾病患者的动脉中层钙化的影响。

Inflammatory, Metabolic, and Coagulation Effects on Medial Arterial Calcification in Patients with Peripheral Arterial Disease.

机构信息

Department of Vascular Diseases, University Medical Centre Ljubljana, 1000 Ljubljana, Slovenia.

Faculty of Medicine, Department of Internal Medicine, University of Ljubljana, 1000 Ljubljana, Slovenia.

出版信息

Int J Mol Sci. 2023 Feb 5;24(4):3132. doi: 10.3390/ijms24043132.

DOI:10.3390/ijms24043132
PMID:36834544
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9962230/
Abstract

Calcium deposits in the vessel wall in the form of hydroxyapatite can accumulate in the intimal layer, as in atherosclerotic plaque, but also in the medial layer, as in medial arterial calcification (MAC) or medial Möenckeberg sclerosis. Once considered a passive, degenerative process, MAC has recently been shown to be an active process with a complex but tightly regulated pathophysiology. Atherosclerosis and MAC represent distinct clinical entities that correlate in different ways with conventional cardiovascular risk factors. As both entities coexist in the vast majority of patients, it is difficult to estimate the relative contribution of specific risk factors to their development. MAC is strongly associated with age, diabetes mellitus, and chronic kidney disease. Given the complexity of MAC pathophysiology, it is expected that a variety of different factors and signaling pathways may be involved in the development and progression of the disease. In this article, we focus on metabolic factors, primarily hyperphosphatemia and hyperglycemia, and a wide range of possible mechanisms by which they might contribute to the development and progression of MAC. In addition, we provide insight into possible mechanisms by which inflammatory and coagulation factors are involved in vascular calcification processes. A better understanding of the complexity of MAC and the mechanisms involved in its development is essential for the development of potential preventive and therapeutic strategies.

摘要

血管壁中的钙沉积以羟磷灰石的形式存在,可在内膜层积聚,如在动脉粥样硬化斑块中,但也可在中膜层积聚,如在中层动脉硬化(MAC)或中层莫恩伯格硬化中。MAC 曾被认为是一种被动的、退行性过程,但最近的研究表明,它是一种具有复杂但受严格调控的病理生理学的主动过程。动脉粥样硬化和 MAC 代表不同的临床实体,它们与传统心血管危险因素以不同的方式相关。由于这两种实体在绝大多数患者中同时存在,因此很难估计特定危险因素对其发展的相对贡献。MAC 与年龄、糖尿病和慢性肾脏病密切相关。鉴于 MAC 病理生理学的复杂性,可以预期,多种不同的因素和信号通路可能参与了疾病的发生和发展。在本文中,我们重点关注代谢因素,主要是高磷血症和高血糖症,以及它们可能导致 MAC 发生和发展的广泛的可能机制。此外,我们还探讨了炎症和凝血因子如何参与血管钙化过程的可能机制。更好地了解 MAC 的复杂性及其发生的机制对于开发潜在的预防和治疗策略至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1630/9962230/085652dca8cb/ijms-24-03132-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1630/9962230/085652dca8cb/ijms-24-03132-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1630/9962230/085652dca8cb/ijms-24-03132-g001.jpg

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