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

Cell Proliferation - Tập 54 Số 3 - 2021
Yuxia Zhang1,2, Ri‐Ning Tang1,2, Liting Wang1,2, Bi‐Cheng Liu1,2
1Institute of Nephrology, Zhongda Hospital, Nanjing Lishui People' Hospital, Nanjing, China
2Institute of Nephrology, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, China

Tóm tắt

AbstractChronic 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.

Từ khóa


Tài liệu tham khảo

10.1056/NEJMoa041031

10.1093/ndt/gfv111

10.18632/aging.102046

Valdivielso JM, 2011, Vascular calcification: types and mechanisms, Nefrologia, 31, 142

10.3390/ijms20225694

10.1186/s12967-017-1190-z

10.3390/toxins12030181

10.1016/j.kint.2016.09.024

10.1093/ndt/gfg414

10.1016/j.kint.2016.09.049

10.1161/ATVBAHA.113.302642

10.1159/000506178

10.1093/cvr/cvy010

10.1111/sdi.12840

10.3390/toxins10060218

10.3389/fphys.2018.00089

10.1161/CIRCULATIONAHA.108.783738

10.1681/ASN.2007121312

10.1159/000504298

10.1016/j.bbrc.2004.05.181

10.1161/JAHA.115.002499

10.3389/fcvm.2018.00027

10.1038/nm.2252

10.1007/s004180100331

10.1161/CIRCRESAHA.113.301792

10.1161/CIRCRESAHA.115.306751

10.1016/j.atherosclerosis.2016.08.046

10.1002/path.5193

10.1093/cvr/cvv221

10.1161/CIRCRESAHA.110.234914

10.3390/toxins11040213

10.1152/ajpcell.00198.2018

10.1016/j.lfs.2015.03.017

10.1371/journal.pone.0147816

10.1186/1475-2840-11-113

10.1186/s12933-016-0358-9

10.1016/j.bbrc.2016.10.027

10.1016/S0140-6736(16)30508-6

Cheng ZY, 2018, Parathyroid hormone promotes osteoblastic differentiation of endothelial cells via the extracellular signal‐regulated protein kinase 1/2 and nuclear factor‐kappaB signaling pathways, Exp Ther Med, 15, 1754

10.1152/ajprenal.00210.2016

10.1038/aps.2016.83

10.1016/S0196-9781(01)00582-4

10.3892/ijmm.2015.2354

10.1016/j.jbiomech.2009.08.006

10.1093/icvts/ivy339

10.1161/ATVBAHA.110.216184

10.1038/s41598-017-03532-z

10.3389/fcvm.2018.00197

10.1093/ndt/gfy325

10.1038/s41598-017-19092-1

10.1097/01.mnh.0000447024.97464.a3

10.1073/pnas.1019219108

10.2174/1389201015666140113113843

10.1016/j.mvr.2008.09.007

10.1152/ajpheart.00075.2010

10.1515/med-2018-0037

10.1159/000330175

10.1159/000493837

10.1016/j.bbrc.2016.01.067

10.1016/j.biocel.2016.06.009

10.1126/science.aau6977

10.1161/ATVBAHA.117.310578

10.4049/jimmunol.1800747

10.1016/j.csbj.2020.04.006

10.1096/fj.14-249706

10.18632/aging.101191

10.1016/j.lfs.2019.116582

10.1186/s13578-018-0263-x

10.1016/j.yjmcc.2016.12.005

10.1161/HYPERTENSIONAHA.116.08459

10.1161/ATVBAHA.117.310490

10.1093/cvr/cvm049

10.1016/j.vph.2016.01.002

10.4061/2011/516237

10.1097/HJH.0000000000001161

10.1016/j.molmed.2019.08.006

10.1152/ajplung.00183.2012

10.1152/ajplung.00091.2011

10.1016/j.bbamem.2012.05.011

10.1159/000445636

10.1182/blood-2006-08-040097

10.1097/FJC.0000000000000567

10.1002/jcb.10583

Thông tin
Thông tin xuất bản

Cell Proliferation

Tập 54 Số 3

Thông tin tác giả