Research progress on T cells in aortic valve calcification

ZHANG Mingdong; LU Zhexin; GU Hongbing; FAN Yongliang; YE Yizhou

doi:10.16766/j.cnki.issn.1674-4152.002999

Volume 21 Issue 5

May 2023

Turn off MathJax

Article Contents

Article Navigation > Chinese Journal of General Practice > 2023 > 21(5): 853-856

ZHANG Mingdong, LU Zhexin, GU Hongbing, FAN Yongliang, YE Yizhou. Research progress on T cells in aortic valve calcification[J]. Chinese Journal of General Practice, 2023, 21(5): 853-856. doi: 10.16766/j.cnki.issn.1674-4152.002999

Citation:

ZHANG Mingdong, LU Zhexin, GU Hongbing, FAN Yongliang, YE Yizhou. Research progress on T cells in aortic valve calcification[J]. Chinese Journal of General Practice, 2023, 21(5): 853-856. doi: 10.16766/j.cnki.issn.1674-4152.002999

Citation:

PDF( 401 KB)

Research progress on T cells in aortic valve calcification

doi: 10.16766/j.cnki.issn.1674-4152.002999

Department of Cardiovascular Surgery, Shanghai First People' s Hospital, Shanghai 201620, China

Received Date: 2022-03-04

Abstract

Abstract

Calcific aortic valve disease (CAVD) is the most common heart valve disease in the world. It is characterized by progressive fibrocalcification of the aortic valve, eventually leading to valve stenosis, heart failure and even death. As research has progressed, CAVD is no longer considered as a simple passive process of calcium deposition in advanced age, but a complex regulatory process involving immune and inflammatory factors. The early pathological mechanism of aortic valve calcification is very similar to the process of atherosclerosis, involving multiple signaling pathways including complex changes such as endothelial injury, lipid infiltration, chronic inflammation, matrix remodeling, cell differentiation, calcium salt deposition, and neovascularization. Recent studies have also highlighted the important regulatory effects of immune and inflammatory responses including oxidized lipids and various cytokines on aortic valve calcification. Immune and inflammatory responses are involved in osteogenesis in the cardiovascular system by regulating bone formation-related signaling pathways leading to aortic valve calcification, in which T cells play a crucial role in its pathogenesis and disease progression. In the process of aortic valve calcification, T cells are regulated by different microenvironmental signals, leading to T cell proliferation and differentiation, with different mechanisms of action. The study of T cell typing and its role in calcified aortic valve will help to explore the treatment methods and prognosis of aortic valve calcification. This article summarizes the current research progress of T cells in aortic valve calcification, and in combination with the research results of T cells in atherosclerosis, explores the potential role of T cells in aortic valve calcification, which may provide a theoretical basis for in-depth research of calcific aortic valve disease and subsequent target drug development.
- Aortic valve calcification,
- Aortic stenosis,
- Immune cells,
- T cells

FullText(HTML)

References(33)

References

[1]	PEETERS F, MEEX S J R, DWECK M R, et al. Calcific aortic valve stenosis: hard disease in the heart: a biomolecular approach towards diagnosis and treatment[J]. Eur Heart J, 2018, 39(28): 2618-2624. doi: 10.1093/eurheartj/ehx653
[2]	CURINI L, ALUSHI B, CHRISTOPHER M R, et al. The first taxonomic and functional characterization of human CAVD-associated microbiota[J]. Microb Cell, 2023, 10(2): 36-48. doi: 10.15698/mic2023.02.791
[3]	RADDATZ M A, MADHUR M S, MERRYMAN W D. Adaptive immune cells in calcific aortic valve disease[J]. Am J Physiol Heart Circ Physiol, 2019, 317(1): H141-H155. doi: 10.1152/ajpheart.00100.2019
[4]	WANG D H, XIONG T H, YU W L, et al. Predicting the key genes involved in aortic valve calcification through integrated bioinformatics analysis[J]. Front Genet, 2021, 12: 650213. DOI: 10.3389/fgene.2021.650213.
[5]	GOLSTEIN P, GRIFFITHS G M. An early history of T cell-mediated cytotoxicity[J]. Nat Rev Immunol, 2018, 18(8): 527-535. doi: 10.1038/s41577-018-0009-3
[6]	PASSOS L S A, JHA P K, BECKER-GREENE D, et al. Prothymosin Alpha: a novel contributor to estradiol receptor alpha-mediated CD8(+) T-cell pathogenic responses and recognition of Type 1 collagen in rheumatic heart valve disease[J]. Circulation, 2022, 145(7): 531-548. doi: 10.1161/CIRCULATIONAHA.121.057301
[7]	NAGY E, LEI Y, MARTíNEZ-MARTíNEZ E, et al. Interferon-γ released by activated CD8(+) T lymphocytes impairs the calcium resorption potential of osteoclasts in calcified human aortic valves[J]. Am J Pathol, 2017, 187(6): 1413-1425. doi: 10.1016/j.ajpath.2017.02.012
[8]	ÉVA SIKURA K, COMBI Z, POTOR L, et al. Hydrogen sulfide inhibits aortic valve calcification in heart via regulating RUNX2 by NF-κB, a link between inflammation and mineralization[J]. J Adv Res, 2021, 27: 165-176. doi: 10.1016/j.jare.2020.07.005
[9]	GRIM J C, AGUADO B A, VOGT B J, et al. Secreted Factors from proinflammatory macrophages promote an osteoblast-like phenotype in valvular interstitial cells[J]. Arterioscler Thromb Vasc Biol, 2020, 40(11): e296-e308.
[10]	WU G F, NIE W B, WANG Q, et al. Umbelliferone ameliorates complete freund adjuvant-induced arthritis via reduction of NF-κB signaling pathway in osteoclast differentiation[J]. Inflammation, 2021, 44(4): 1315-1329. doi: 10.1007/s10753-021-01418-x
[11]	HE Y B, GUO J H, WANG C, et al. IL-33 promotes the progression of nonrheumatic aortic valve stenosis via inducing differential phenotypic transition in valvular interstitial cells[J]. J Cardiol, 2020, 75(2): 124-133. doi: 10.1016/j.jjcc.2019.06.011
[12]	MERINO-MERINO A, GONZALEZ-BERNAL J, FERNANDEZ-ZOPPINO D, et al. The role of Galectin-3 and ST2 in cardiology: a short review[J]. Biomolecules, 2021, 11(8): 1167. doi: 10.3390/biom11081167
[13]	SCHNITZLER J G, ALI L, GROENEN A G, et al. Lipoprotein(a) as orchestrator of calcific aortic valve stenosis[J]. Biomolecules, 2019, 9(12): 760. doi: 10.3390/biom9120760
[14]	CHEN X, WANG Z Q, DUAN N, et al. Osteoblast-osteoclast interactions[J]. Connect Tissue Res, 2018, 59(2): 99-107. doi: 10.1080/03008207.2017.1290085
[15]	ALLAM G, ABDEL-MONEIM A, GABER A M. The pleiotropic role of interleukin-17 in atherosclerosis[J]. Biomed Pharmacother, 2018, 106: 1412-1418. doi: 10.1016/j.biopha.2018.07.110
[16]	LJUNGBERG J, JANIEC M, BERGDAHL I A, et al. Proteomic biomarkers for incident aortic stenosis requiring valvular replacement[J]. Circulation, 2018, 138(6): 590-599. doi: 10.1161/CIRCULATIONAHA.117.030414
[17]	LIU Z T, WANG Y X, SHI J W, et al. IL-21 promotes osteoblastic differentiation of human valvular interstitial cells through the JAK3/STAT3 pathway[J]. Int J Med Sci, 2020, 17(18): 3065-3072. doi: 10.7150/ijms.49533
[18]	SAIGUSA R, WINKELS H, LEY K. T cell subsets and functions in atherosclerosis[J]. Nat Rev Cardiol, 2020, 17(7): 387-401. doi: 10.1038/s41569-020-0352-5
[19]	MUNJAL A, KHANDIA R. Atherosclerosis: orchestrating cells and biomolecules involved in its activation and inhibition[J]. Adv Protein Chem Struct Biol, 2020, 120: 85-122. http://www.xueshufan.com/publication/2996257806
[20]	CROTTY S. T follicular helper cell biology: a decade of discovery and diseases[J]. Immunity, 2019, 50(5): 1132-1148. doi: 10.1016/j.immuni.2019.04.011
[21]	GADDIS D E, PADGETT L E, WU R P, et al. Apolipoprotein AI prevents regulatory to follicular helper T cell switching during atherosclerosis[J]. Nat Commun, 2018, 9(1): 1095. doi: 10.1038/s41467-018-03493-5
[22]	TAY C, LIU Y H, KANELLAKIS P, et al. Follicular B cells promote atherosclerosis via T cell-mediated differentiation into plasma cells and secreting pathogenic immunoglobulin g[J]. Arterioscler Thromb Vasc Biol, 2018, 38(5): e71-e84.
[23]	SAITO T. Molecular dynamics of co-signal molecules in T-Cell activation[J]. Adv Exp Med Biol, 2019, 1189: 135-152.
[24]	余筱燕, 汤珂珂, 吕迪. 阻滞Kv1.3通道抑制CD4⁺ CD28(null) T细胞活性缓解糖尿病微血管损伤的实验研究[J]. 中华全科医学, 2019, 17(8): 1335-1339, 1412. doi: 10.16766/j.cnki.issn.1674-4152.000937 YU X Y, TANG K K, LYU D. Inhibit the activity of CD4⁺ CD28null T cells to alleviate diabetic microvascular damage by blocking Kv1.3 channel[J]. Chinese Journal of General Practice, 2019, 17(8): 1335-1339, 1412. doi: 10.16766/j.cnki.issn.1674-4152.000937
[25]	BROADLEY I, PERA A, MORROW G, et al. Expansions of Cytotoxic CD4⁺CD28^- T cells drive excess cardiovascular mortality in rheumatoid arthritis and other chronic inflammatory conditions and are triggered by CMV infection[J]. Front Immunol, 2017, 8: 195.
[26]	VAN LAECKE S, MALFAIT T, SCHEPERS E, et al. Cardiovascular disease after transplantation: an emerging role of the immune system[J]. Transpl Int, 2018, 31(7): 689-699. doi: 10.1111/tri.13160
[27]	LEE S, BARTLETT B, DWIVEDI G. Adaptive immune responses in human atherosclerosis[J]. Int J Mol Sci, 2020, 21(23): 9322. doi: 10.3390/ijms21239322
[28]	FU Y, LIN Q, ZHANG Z R, et al. Therapeutic strategies for the costimulatory molecule OX40 in T-cell-mediated immunity[J]. Acta Pharm Sin B, 2020, 10(3): 414-433. doi: 10.1016/j.apsb.2019.08.010
[29]	DUAN Y Y, TANG H Y, MITCHELL-SILBAUGH K, et al. Heat shock protein 60 in cardiovascular physiology and diseases[J]. Front Mol Biosci, 2020, 7: 73. doi: 10.3389/fmolb.2020.00073
[30]	ABEL A M, YANG C, THAKAR M S, et al. Natural killer cells: development, maturation, and clinical utilization[J]. Front Immunol, 2018, 9: 1869. doi: 10.3389/fimmu.2018.01869
[31]	MAZUR P, MIELIMONKA A, NATORSKA J, et al. Lymphocyte and monocyte subpopulations in severe aortic stenosis at the time of surgical intervention[J]. Cardiovasc Pathol, 2018, 35: 1-7. doi: 10.1016/j.carpath.2018.03.004
[32]	BLASER M C, KRALER S, LVSCHER T F, et al. Multi-Omics approaches to define calcific aortic valve disease pathogenesis[J]. Circ Res, 2021, 128(9): 1371-1397. doi: 10.1161/CIRCRESAHA.120.317979
[33]	SHARMA N, TOOR D. Interleukin-10: role in increasing susceptibility and pathogenesis of rheumatic fever/rheumatic heart disease[J]. Cytokine, 2017, 90: 169-176. doi: 10.1016/j.cyto.2016.11.010

Relative Articles

Supplements(0)

Cited By

Proportional views

Proportional views

通讯作者: 陈斌, bchen63@163.com

1.
沈阳化工大学材料科学与工程学院沈阳 110142

Get Citation

PDF

XML

Article Metrics

Article views (252) PDF downloads(14)

Research progress on T cells in aortic valve calcification

doi: 10.16766/j.cnki.issn.1674-4152.002999

Abstract

References

Proportional views

Catalog

通讯作者: 陈斌, bchen63@163.com

Article Metrics

Proportional views

Related

Research progress on T cells in aortic valve calcification

doi: 10.16766/j.cnki.issn.1674-4152.002999

Abstract

References

Proportional views

Catalog

通讯作者: 陈斌, bchen63@163.com

Article Metrics

Proportional views

Related

Export File

Citation

Format

Content