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中华肾病研究电子杂志 ›› 2023, Vol. 12 ›› Issue (04) : 234 -237. doi: 10.3877/cma.j.issn.2095-3216.2023.04.011

综述

巨噬细胞在慢性肾脏病患者血管钙化中的作用与机制研究进展
金艳盛, 董改琴, 李晓忠()   
  1. 215025 苏州大学附属儿童医院肾脏免疫科
  • 收稿日期:2022-12-19 出版日期:2023-08-28
  • 通信作者: 李晓忠
  • 基金资助:
    苏州市医学重点学科(SZXK202106); 苏州市科技计划项目(SKYD2022072、SS202067)

Progress of research on the role and mechanism of macrophages in vascular calcification of patients with chronic kidney disease

Yansheng Jin, Gaiqin Dong, Xiaozhong Li()   

  1. Department of Nephrology and Immunology, Children′s Hospital Affiliated to Soochow University, Suzhou 215025, Jiangsu Province, China
  • Received:2022-12-19 Published:2023-08-28
  • Corresponding author: Xiaozhong Li
引用本文:

金艳盛, 董改琴, 李晓忠. 巨噬细胞在慢性肾脏病患者血管钙化中的作用与机制研究进展[J/OL]. 中华肾病研究电子杂志, 2023, 12(04): 234-237.

Yansheng Jin, Gaiqin Dong, Xiaozhong Li. Progress of research on the role and mechanism of macrophages in vascular calcification of patients with chronic kidney disease[J/OL]. Chinese Journal of Kidney Disease Investigation(Electronic Edition), 2023, 12(04): 234-237.

血管钙化(VC)是慢性肾脏病(CKD)患者的心血管事件发病率和病死率增加的重要因素。已有研究表明巨噬细胞在VC发生、发展和消退中起着关键的调节作用。然而,巨噬细胞在CKD患者VC中的作用与机制尚未完全清楚。本文就巨噬细胞在CKD相关VC中的作用与机制研究进展作一综述,旨在为防治CKD患者的VC提供新思路。

Vascular calcification (VC) is an important factor for the increase of both incidence of cardiovascular events and mortality in patients with chronic kidney disease (CKD). Previous studies have shown that macrophages played a key regulatory role in the occurrence, development, and regression of VC. However, the role and mechanism of macrophages in VC of CKD patients are not fully understood. This article reviewed the progress of research on the role and mechanism of macrophages in CKD-related VC with the aim of providing new ideas for the prevention and treatment of VC in CKD patients.

图1 巨噬细胞促进和抑制慢性肾脏病血管钙化的作用机制
图2 硫酸吲哚酚和磷酸盐调控巨噬细胞功能影响血管钙化注:RANKL:receptor activator of NF-κB ligand,NF-κB受体激活剂配体;RANK: NF-κB的受体激活剂;CA2:carbonic anhydrase 2,碳酸酐酶2
[1]
Dube P, DeRiso A, Patel M, et al. Vascular calcification in chronic kidney disease: diversity in the vessel wall [J]. Biomedicines, 2021, 9(4): 404.
[2]
杨璨粼,张晓良. SNF472:一种新型血管钙化和钙化防御治疗药物[J]. 中华肾脏病杂志2022, 38(11): 1011-1015.
[3]
Passos L, Lupieri A, Becker-Greene D, et al. Innate and adaptive immunity in cardiovascular calcification [J]. Atherosclerosis, 2020, 306: 59-67.
[4]
Li Y, Sun Z, Zhang L, et al. Role of macrophages in the progression and regression of vascular calcification [J]. Front Pharmacol, 2020, 11: 661.
[5]
Hénaut L, Candellier A, Boudot C, et al. New insights into the roles of monocytes/macrophages in cardiovascular calcification associated with chronic kidney disease [J]. Toxins (Basel), 2019, 11(9): 529.
[6]
Reinhold S, Blankesteijn WM, Foulquier S. The interplay of WNT and PPARγ signaling in vascular calcification [J]. Cells, 2020, 9(12): 2658.
[7]
Talwar S, Kant A, Xu T, et al. Mechanosensitive smooth muscle cell phenotypic plasticity emerging from a null state and the balance between Rac and Rho [J]. Cell Rep, 2021, 35(3): 109019.
[8]
Lee CF, Carley RE, Butler CA, et al. Rac GTPase signaling in immune-mediated mechanisms of atherosclerosis [J]. Cells, 2021, 10(11): 2808.
[9]
Healy A, Berus JM, Christensen JL, et al. Statins disrupt macrophage Rac1 regulation leading to increased atherosclerotic plaque calcification [J]. Arterioscler Thromb Vasc Biol, 2020, 40(3): 714-732.
[10]
Jäger E, Murthy S, Schmidt C, et al. Calcium-sensing receptor-mediated NLRP3 inflammasome response to calciprotein particles drives inflammation in rheumatoid arthritis [J]. Nat Commun, 2020, 11(1): 4243.
[11]
Cobb AM, Yusoff S, Hayward R, et al. Runx2 (Runt-related transcription factor 2) links the DNA damage response to osteogenic reprogramming and apoptosis of vascular smooth muscle cells [J]. Arterioscler Thromb Vasc Biol, 2021, 41(4): 1339-1357.
[12]
Waring OJ, Skenteris NT, Biessen E, et al. Two-faced Janus: the dual role of macrophages in atherosclerotic calcification [J]. Cardiovasc Res, 2022, 118(13): 2768-2777.
[13]
于涵,王保兴. 慢性肾脏病血管钙化的分子机制研究进展[J/CD]. 中华肾病研究电子杂志2021, 10(4): 232-235.
[14]
Dube PR, Chikkamenahalli LL, Birnbaumer L, et al. Reduced calcification and osteogenic features in advanced atherosclerotic plaques of mice with macrophage-specific loss of TRPC3 [J]. Atherosclerosis, 2018, 270: 199-204.
[15]
Liu L, Zeng P, Yang X, et al. Inhibition of vascular calcification [J]. Arterioscler Thromb Vasc Biol, 2018, 38(10): 2382-2395.
[16]
Li P, Wang Y, Liu X, et al. Loss of PARP-1 attenuates diabetic arteriosclerotic calcification via Stat1/Runx2 axis [J]. Cell Death Dis, 2020, 11(1): 22.
[17]
Yaker L, Tebani A, Lesueur C, et al. Extracellular vesicles from LPS-treated macrophages aggravate smooth muscle cell calcification by propagating inflammation and oxidative stresss [J]. Front Cell Dev Biol, 2022, 10: 823450.
[18]
Rogers MA, Buffolo F, Schlotter F, et al. Annexin A1-dependent tethering promotes extracellular vesicle aggregation revealed with single-extracellular vesicle analysis [J]. Sci Adv, 2020, 6(38): eabb1244.
[19]
Kawakami R, Katsuki S, Travers R, et al. S100A9-RAGE axis accelerates formation of macrophage-mediated extracellular vesicle microcalcification in diabetes mellitus [J]. Arterioscler Thromb Vasc Biol, 2020, 40(8): 1838-1853.
[20]
Jing L, Li L, Sun Z, et al. Role of matrix vesicles in bone-vascular cross-talk [J]. J Cardiovasc Pharmacol, 2019, 74(5): 372-378.
[21]
Villa-Bellosta R. New insights into endogenous mechanisms of protection against arterial calcification [J]. Atherosclerosis, 2020, 306: 68-74.
[22]
Schloesser D, Lindenthal L, Sauer J, et al. Senescent cells suppress macrophage-mediated corpse removal via upregulation of the CD47-QPCT/L axis [J]. J Cell Biol, 2023, 222(2): e202207097.
[23]
Sha X, Dai Y, Chong L, et al. Pro-efferocytic macrophage membrane biomimetic nanoparticles for the synergistic treatment of atherosclerosis via competition effect [J]. J Nanobiotechnology, 2022, 20(1): 506.
[24]
Simpson CL, Mosier JA, Vyavahare NR. Osteoclast-mediated cell therapy as an attempt to treat elastin specific vascular calcification [J]. Molecules, 2021, 26(12): 3643.
[25]
Yang D, Wan Y. Molecular determinants for the polarization of macrophage and osteoclast [J]. Semin Immunopathol, 2019, 41(5): 551-563.
[26]
Ishida K, Ashizawa N, Matsumoto K, et al. Novel bisphosphonate compound FYB-931 preferentially inhibits aortic calcification in vitamin D3-treated rats [J]. J Bone Miner Metab, 2019, 37(5): 796-804.
[27]
何叶梅,欧三桃. 硫酸吲哚酚与血管钙化的关系的研究进展[J]. 医学研究生学报2021, 34(11): 1228-1232.
[28]
Maheshwari V, Tao X, Thijssen S, et al. Removal of protein-bound uremic toxins using binding competitors in hemodialysis: a narrative review [J]. Toxins (Basel), 2021, 13(9): 622.
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