Role of crosstalk between endothelial cells and smooth muscle cells in vascular calcification in chronic kidney disease,Cell Proliferation

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Role of crosstalk between endothelial cells and smooth muscle cells in vascular calcification in chronic kidney disease
Cell Proliferation ( IF 5.9 ) Pub Date : 2021-01-27 , DOI: 10.1111/cpr.12980
Yu‐Xia Zhang _{1,

2} , Ri‐Ning Tang _{1,

2} , Li‐Ting Wang _{1,

2} , Bi‐Cheng Liu _{1,

2}

Affiliation

Chronic kidney disease (CKD) is a severe health problem worldwide, and vascular calcification (VC) contributes substantially to the cardiovascular morbidity and high mortality of CKD. CKD is often accompanied by a variety of pathophysiological states, such as inflammation, oxidative stress, hyperglycaemia, hyperparathyroidism and haemodynamic derangement, that can cause injuries to smooth muscle cells (SMCs) and endothelial cells (ECs) to promote VC. Similar to SMCs, whose role has been widely explored in VC, ECs may contribute to VC via osteochondral transdifferentiation, apoptosis, etc. In addition, given their location in the innermost layer of the blood vessel lumen and preferential reception of various pro‐calcification stimuli, ECs can pass messages to vascular wall cells and communicate with them. Crosstalk between ECs and SMCs via cytokines through a paracrine mechanism, extracellular vesicles, miRNAs and myoendothelial gap junctions also plays a role in VC. In this review, we emphasize the role of intercellular crosstalk between ECs and SMCs in VC associated with CKD.

中文翻译：

内皮细胞和平滑肌细胞之间的串扰在慢性肾脏疾病中的血管钙化中的作用

慢性肾脏病（CKD）是世界范围内的严重健康问题，而血管钙化（VC）在很大程度上导致了CKD的心血管疾病和高死亡率。CKD通常伴有多种病理生理状态，例如炎症，氧化应激，高血糖症，甲状旁腺功能亢进和血流动力学紊乱，可导致平滑肌细胞（SMC）和内皮细胞（EC）损伤，从而促进VC。类似于在VC中已广泛研究其作用的SMC，EC可能通过骨软骨转分化，凋亡等促进VC。此外，由于它们位于血管内腔的最内层并优先接受各种促钙化刺激EC可以将消息传递到血管壁细胞并与其进行通信。EC和SMC通过旁分泌机制通过细胞因子之间的串扰，细胞外囊泡，miRNA和肌内皮间隙连接在VC中也起作用。在这篇综述中，我们强调了EC和SMC之间的细胞间串扰在与CKD相关的VC中的作用。

更新日期：2021-03-09

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