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

doi:10.3877/cma.j.issn.2095-3216.2023.04.011

Abstract

Abstract:

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.

Key words: Macrophage, Vascular calcification, Chronic kidney disease

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]. Chinese Journal of Kidney Disease Investigation(Electronic Edition), 2023, 12(04): 234-237.

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References 28

[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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