Role of smooth muscle cells in vascular calcification: implications in atherosclerosis and arterial stiffness.
Role of smooth muscle cells in vascular calcification: implications in atherosclerosis and arterial stiffness.
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DOI：
10.1093/cvr/cvy010
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发表时间：
2018-03-15
影响因子：
10.8
通讯作者：
Shanahan CM
中科院分区：
文献类型：
--
作者：
Durham AL;Speer MY;Scatena M;Giachelli CM;Shanahan CM
血管钙化与全因死亡率和动脉粥样硬化斑块破裂显著增加相关。钙化已被确定为部分由血管壁内的血管平滑肌细胞（VSMC）转分化驱动的主动过程。历史上，VSMC表型转换被认为是二元的，细胞能够采用生理收缩表型或替代的“合成”表型来响应损伤。然而，最近的工作，包括谱系追踪，揭示了VSMC能够采用许多表型，包括钙化（成骨、软骨细胞和骨细胞）、脂肪形成和巨噬细胞表型。虽然驱动VSMC分化的机制仍在阐明，但越来越清楚的是，中膜钙化可能在几个方面与动脉粥样硬化病变中观察到的内膜钙化不同，包括VSMC表型变化和钙化的风险因素和特定驱动因素。本文旨在比较和对比血管平滑肌细胞在动脉粥样硬化和血管介质中驱动钙化的作用，重点关注钙化的主要驱动因素，包括衰老，尿毒症，机械应激，氧化应激和炎症。该综述还讨论了新的发现，也引起了人们的注意，具体的亲和抗钙化蛋白，细胞外囊泡，线粒体功能障碍，和尿毒症环境血管钙化的主要决定因素。
Vascular calcification is associated with a significant increase in all-cause mortality and atherosclerotic plaque rupture. Calcification has been determined to be an active process driven in part by vascular smooth muscle cell (VSMC) transdifferentiation within the vascular wall. Historically, VSMC phenotype switching has been viewed as binary, with the cells able to adopt a physiological contractile phenotype or an alternate ‘synthetic’ phenotype in response to injury. More recent work, including lineage tracing has however revealed that VSMCs are able to adopt a number of phenotypes, including calcific (osteogenic, chondrocytic, and osteoclastic), adipogenic, and macrophagic phenotypes. Whilst the mechanisms that drive VSMC differentiation are still being elucidated it is becoming clear that medial calcification may differ in several ways from the intimal calcification seen in atherosclerotic lesions, including risk factors and specific drivers for VSMC phenotype changes and calcification. This article aims to compare and contrast the role of VSMCs in driving calcification in both atherosclerosis and in the vessel media focusing on the major drivers of calcification, including aging, uraemia, mechanical stress, oxidative stress, and inflammation. The review also discusses novel findings that have also brought attention to specific pro- and anti-calcifying proteins, extracellular vesicles, mitochondrial dysfunction, and a uraemic milieu as major determinants of vascular calcification.
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影响因子：
5.5
作者：
Chiong M;Cartes-Saavedra B;Norambuena-Soto I;Mondaca-Ruff D;Morales PE;García-Miguel M;Mellado R
通讯作者：
Mellado R
影响因子：
4.3
作者：
Byon, Chang Hyun;Chen, Yabing
通讯作者：
Chen, Yabing
影响因子：
20.1
作者：
Cheng SL;Ramachandran B;Behrmann A;Shao JS;Mead M;Smith C;Krchma K;Bello Arredondo Y;Kovacs A;Kapoor K;Brill LM;Perera R;Williams BO;Towler DA
通讯作者：
Towler DA
影响因子：
3.3
作者：
Beloqui, Oscar;Moreno, Maria U.;Zalba, Guillermo
通讯作者：
Zalba, Guillermo
影响因子：
4.8
作者：
Byon, Chang Hyun;Javed, Amjad;Chen, Yabing
通讯作者：
Chen, Yabing