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This article is a review on calcified aortic lesions, clarifying that arteries are the second most common calcified structure in the human body after bones. It systematically elaborates on the occurrence patterns, tissue anatomical characteristics, and pathological correlations of aortic calcification under the influence of aging and damage; it reveals the core regulatory roles of innate immunity participation, aging-related inflammatory responses, and ectopic activation of bone formation mechanisms during the lesion process; it integrates recent basic research findings and summarizes the response characteristics and intrinsic biological laws of the lesion to aging and damage, thereby improving the basic understanding of aortic calcification deposition.
This review addresses the regenerative and repair challenges caused by the heterogeneity of bone-cartilage tissue, with the tissue engineering system combining mesenchymal stem cells and biomaterial scaffolds as the core. It clarifies the regulatory mechanism of biological physical signals on the fate of stem cells, systematically summarizes the progress in the design of biomimetic microenvironment scaffolds under mechanical biology guidance, and achieves precise regulation of the lineage-specific differentiation of mesenchymal stem cells, providing theoretical support and design references for layered bone-cartilage regeneration, especially for the regeneration of subchondral bone.
01 Research Background
Arteries in the human body are the second most common calcified structure after bones. Aortic and aortic valve calcification are prevalent in specific social populations; age is an important influencing factor, and aortic calcification usually occurs earlier than thoracic aortic calcification. Under the condition of accompanying metabolic, mechanical or inflammatory damage, heart valves and thoracic aortic calcification may occur prematurely, and such calcification often involves the arterial media, and is closely related to premature aging, accelerated neurocognitive decline, and adverse cardiovascular outcomes. The concept of atherosclerosis has been proposed for nearly two centuries to describe the age-related aortic calcification-mediated hardening phenomenon, while the systematic understanding of the causes, characteristics, and pathological effects of aortic calcification deposition has only gradually formed in the past decade. Key biological characteristics such as innate immune regulation, aging-related inflammation, and ectopic activation of bone formation mechanisms have been continuously revealed.
The tendon-bone transitional tissue has a highly specialized extracellular matrix structure, with the core feature being the hierarchical arrangement of collagen and the gradient composition of minerals. This structural system can achieve stable force transmission and guide the cell phenotype of the spatial organization. Currently, it is impossible to precisely reproduce the complex multi-scale structure and composition gradient at the tendon-bone interface, which has become a key bottleneck hindering the integration and regeneration of soft and hard tissue interfaces, and requires the development of biomimetic matrix construction schemes that conform to the characteristics of natural structures.
02 Main Content
This article focuses on the response of calcified aortic lesions to aging and damage as the core direction, comprehensively reviewing relevant research literature; it clarifies the temporal sequence, inducing conditions, and tissue anatomical characteristics of aortic calcification in different locations; it focuses on the core biological mechanisms of the lesion, highlighting the participation patterns of the innate immune system, the pathogenic pathways of aging-related inflammation, and the ectopic activation process of bone formation-related mechanisms; it analyzes the intrinsic association between calcified aortic lesions and premature aging phenotypes, integrating the latest discoveries from basic exploration, and improving the understanding of the pathological process of the lesion.
03 Research Design
This study is a review-type research, with aging and damage as the core thread, integrating recent published basic scientific exploration results, and conducting a systematic review, summary, and analysis of the occurrence patterns, tissue anatomical characteristics, pathological correlations, and core biological mechanisms (focusing on ectopic activation of bone formation mechanisms) of calcified aortic lesions, to construct a framework for the basic mechanism cognition of the lesion.
04 Results
Arteries are the second most common calcified structure in the human body, and aortic calcification presents a site-specific temporal sequence characteristic with age; metabolic, mechanical, and inflammatory damage factors can trigger aortic and thoracic aortic calcification prematurely, and the lesion often involves the arterial media, and is significantly associated with premature aging phenotypes. The pathological process of calcified aortic lesions is regulated by multiple mechanisms. The innate immune system is involved, and the senescence-related inflammatory response promotes the development of the lesion. The ectopic activation of bone formation-related mechanisms also mediates the occurrence and progression of aortic calcium deposition. The understanding of the basic biological laws and internal mechanisms of aortic calcium deposition by the academic community has been comprehensively supplemented and improved in recent years.
DOI：10.1161/circulationaha.125.072393
