Medial arterial calcification (MAC) is a chronic systemic vascular disorder distinct from atherosclerosis that is frequently but not always associated with diabetes mellitus, chronic kidney disease, and aging. MAC is also a part of more complex phenotypes in numerous less common diseases. The hallmarks of MAC include disseminated and progressive precipitation of calcium phosphate within the medial layer, a prolonged and clinically silent course, and compromise of hemodynamics associated with chronic limb-threatening ischemia. MAC increases the risk of complications during vascular interventions and mitigates their outcomes. With the exception of rare monogenetic defects affecting adenosine triphosphate metabolism, MAC pathogenesis remains unknown, and causal therapy is not available. Implementation of genetics and omics-based approaches in research recognizing the critical importance of calcium phosphate thermodynamics holds promise to unravel MAC molecular pathogenesis and to provide guidance for therapy. The current state of knowledge concerning MAC is reviewed, and future perspectives are outlined.

内侧动脉钙化（MAC）是一种与动脉粥样硬化不同的慢性全身性血管疾病，经常但并不总是与糖尿病、慢性肾病和衰老相关。MAC 也是许多不太常见疾病中更复杂表型的一部分。MAC 的特征包括内侧层内磷酸钙的播散性和渐进性沉淀、长期且临床无症状的病程以及与慢性肢体威胁性缺血相关的血流动力学损害。MAC 会增加血管介入治疗期间并发症的风险并减轻其结果。除了影响三磷酸腺苷代谢的罕见单基因缺陷外，MAC 的发病机制仍不清楚，并且无法找到病因治疗方法。在认识到磷酸钙热力学的至关重要性的研究中实施基于遗传学和组学的方法有望解开 MAC 分子发病机制并为治疗提供指导。回顾了有关 MAC 的知识现状，并概述了未来的前景。