Mechanisms underlying the TNF-α-mediated inflammatory response in calcific aortic valve disease
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摘要: 钙化性主动脉瓣膜病是以主动脉瓣叶纤维化、钙化为特征的进展性心血管疾病,炎症反应是主动脉瓣钙化发生发展的重要机制。肿瘤坏死因子-α(TNF-α)是一类重要的炎性递质,通过多重炎症信号通路加剧疾病的进展。本文主要综述TNF-α介导的炎症反应在钙化性主动脉瓣膜病中的作用机制及研究进展,为该病的临床治疗提供新思路。Abstract: Calcific aortic valve disease is a progressive cardiovascular condition characterized by fibrosis and calcification of the aortic valve. The inflammatory response plays a crucial role in the development and progression of aortic valve calcification. Tumor necrosis factor-α(TNF-α) is a key inflammatory mediator, that accelerates disease progression through various inflammatory signaling pathways. This paper provides a comprehensive review of the mechanisms and recent research advancements concerning TNF-α-mediated inflammatory responses in calcific aortic valve disease, offering novel perspectives for clinical treatment strategies.
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[1] Roth GA, Mensah GA, Johnson CO, et al. Global burden of cardiovascular diseases and risk factors, 1990-2019: update from the GBD 2019 study[J]. J Am Coll Cardiol, 2020, 76(25): 2982-3021. doi: 10.1016/j.jacc.2020.11.010
[2] Lutz M, Messika-Zeitoun D, Rudolph TK, et al. Differences in the presentation and management of patients with severe aortic stenosis in different European centres[J]. Open Heart, 2020, 7(2): e001345. doi: 10.1136/openhrt-2020-001345
[3] Yi B, Zeng W, Lv L, et al. Changing epidemiology of calcific aortic valve disease: 30-year trends of incidence, prevalence, and deaths across 204 countries and territories[J]. Aging(Albany NY), 2021, 13(9): 12710-12732.
[4] 王世杰, 刘鹏, 温姝钰, 等. 主动脉瓣疾病手术治疗现状与进展[J]. 临床心血管病杂志, 2023, 39(6): 417-424. doi: 10.13201/j.issn.1001-1439.2023.06.003
[5] 张航, 王华君, 石凤梧, 等. 经导管主动脉瓣置换术冠状动脉阻塞风险预防的单中心研究[J]. 临床心血管病杂志, 2024, 40(8): 652-655. doi: 10.13201/j.issn.1001-1439.2024.08.009
[6] 王圣, 陈现杰, 陆国庆, 等. 胸骨旁切口微创主动脉瓣置换的围术期指标观察[J]. 临床心血管病杂志, 2024, 40(11): 918-922. doi: 10.13201/j.issn.1001-1439.2024.11.011
[7] Vahanian A, Beyersdorf F, Praz F, et al. 2021 ESC/EACTS Guidelines for the management of valvular heart disease[J]. Eur Heart J, 2022;43(7): 561-632. doi: 10.1093/eurheartj/ehab395
[8] Kovacic JC, Dimmeler S, Harvey RP, et al. Endothelial to mesenchymal transition in cardiovascular disease: JACC state-of-the-art review[J]. J Am Coll Cardiol, 2019, 73(2): 190-209. doi: 10.1016/j.jacc.2018.09.089
[9] Xiao F, Pan H, Yang D, et al. Identification of TNFα-mediated inflammation as potential pathological marker and therapeutic target for calcification progress of congenital bicuspid aortic valve[J]. Eur J Pharmacol, 2023, 951: 175783. doi: 10.1016/j.ejphar.2023.175783
[10] Towler DA. Molecular and cellular aspects of calcific aortic valve disease[J]. Circ Res, 2013, 113(2): 198-208. doi: 10.1161/CIRCRESAHA.113.300155
[11] Huang Y, Wang C, Zhou T, et al. Lumican promotes calcific aortic valve disease through H3 histone lactylation[J]. Eur Heart J, 2024, 45(37): 3871-3885. doi: 10.1093/eurheartj/ehae407
[12] Otto CM, Newby DE, Hillis GS. Calcific aortic stenosis: a review[J]. JAMA, 2024, 332(23): 2014-2026. doi: 10.1001/jama.2024.16477
[13] Dutta P, Lincoln J. Calcific aortic valve disease: a developmental biology perspective[J]. Curr Cardiol Rep, 2018, 20(4): 21. doi: 10.1007/s11886-018-0968-9
[14] Artiach G, Carracedo M, Plunde O, et al. Omega-3 polyunsaturated fatty acids decrease aortic valve disease through the resolvin E1 and ChemR23 axis[J]. Circulation, 2020, 142(8): 776-789. doi: 10.1161/CIRCULATIONAHA.119.041868
[15] Jang DI, Lee AH, Shin HY, et al. The role of tumor necrosis factor alpha(TNF-α)in autoimmune disease and current TNF-α inhibitors in therapeutics[J]. Int J Mol Sci, 2021, 22(5): 2719. doi: 10.3390/ijms22052719
[16] Gee T, Farrar E, Wang Y, et al. NFκB(nuclear factor κ-light-chain enhancer of activated B Cells)activity regulates cell-type-specific and context-specific susceptibility to calcification in the aortic valve[J]. Arterioscler Thromb Vasc Biol, 2020, 40(3): 638-655. doi: 10.1161/ATVBAHA.119.313248
[17] Bossé Y, Miqdad A, Fournier D, et al. Refining molecular pathways leading to calcific aortic valve stenosis by studying gene expression profile of normal and calcified stenotic human aortic valves[J]. Circ Cardiovasc Genet, 2009, 2(5): 489-498. doi: 10.1161/CIRCGENETICS.108.820795
[18] Coté N, Mahmut A, Bosse Y, et al. Inflammation is associated with the remodeling of calcific aortic valve disease[J]. Inflammation, 2013, 36(3): 573-581. doi: 10.1007/s10753-012-9579-6
[19] Isoda K, Matsuki T, Kondo H, et al. Deficiency of interleukin-1 receptor antagonist induces aortic valve disease in BALB/c mice[J]. Arterioscler Thromb Vasc Biol, 2010, 30(4): 708-715. doi: 10.1161/ATVBAHA.109.201749
[20] Fernandez Esmerats J, Villa-Roel N, Kumar S, et al. Disturbed flow increases UBE2C(Ubiquitin E2 Ligase C)via loss of miR-483-3p, inducing aortic valve calcification by the pVHL(von Hippel-Lindau protein)and HIF-1α(hypoxia-inducible factor-1α)pathway in endothelial cells[J]. Arterioscler Thromb Vasc Biol, 2019, 39(3): 467-481. doi: 10.1161/ATVBAHA.118.312233
[21] Sánchez-Duffhues G, García de Vinuesa A, van de Pol V, et al. Inflammation induces endothelial-to-mesenchymal transition and promotes vascular calcification through downregulation of BMPR2[J]. J Pathol, 2019, 247(3): 333-346. doi: 10.1002/path.5193
[22] Thériault S, Dina C, Messika-Zeitoun D, et al. Genetic association analyses highlight IL6, ALPL, and NAV1 as 3 new susceptibility genes underlying calcific aortic valve stenosis[J]. Circ Genom Precis Med, 2019, 12(10): e002617. doi: 10.1161/CIRCGEN.119.002617
[23] Zhang J, Alcaide P, Liu L, et al. Regulation of endothelial cell adhesion molecule expression by mast cells, macrophages, and neutrophils[J]. PLoS One, 2011, 6(1): e14525. doi: 10.1371/journal.pone.0014525
[24] Xu K, Zhou T, Huang Y, et al. Anthraquinone emodin inhibits tumor necrosis factor alpha-induced calcification of human aortic valve interstitial cells via the NF-κB pathway[J]. Front Pharmacol, 2018, 9: 1328. doi: 10.3389/fphar.2018.01328
[25] 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
[26] Combi Z, Potor L, Nagy P, et al. Hydrogen sulfide as an anti-calcification stratagem in human aortic valve: Altered biogenesis and mitochondrial metabolism of H(2) S lead to H(2) S deficiency in calcific aortic valve disease[J]. Redox Biol, 2023, 60: 102629. doi: 10.1016/j.redox.2023.102629
[27] Wu J, Huang H, Yang W, et al. TRPM4 mRNA stabilization by METTL3-mediated m6A modification promotes calcific aortic valve inflammation[J]. Heliyon, 2024, 10(11): e31871. doi: 10.1016/j.heliyon.2024.e31871
[28] Zhang P, The E, Luo Z, et al. Pro-inflammatory mediators released by activated monocytes promote aortic valve fibrocalcific activity[J]. Mol Med, 2022, 28(1): 5. doi: 10.1186/s10020-022-00433-4
[29] Huang G, An L, Fan M, et al. Potential role of full-length and nonfull-length progranulin in affecting aortic valve calcification[J]. J Mol Cell Cardiol, 2020, 141: 93-104. doi: 10.1016/j.yjmcc.2020.03.012
[30] Wang C, Xia Y, Qu L, et al. Cardamonin inhibits osteogenic differentiation of human valve interstitial cells and ameliorates aortic valve calcification via interfering in the NF-κB/NLRP3 inflammasome pathway[J]. Food Funct, 2021, 12(23): 11808-11818. doi: 10.1039/D1FO00813G
[31] Passos LSA, Lupieri A, Becker-Greene D, et al. Innate and adaptive immunity in cardiovascular calcification[J]. Atherosclerosis, 2020, 306: 59-67. doi: 10.1016/j.atherosclerosis.2020.02.016
[32] Zhang P, The E, Nedumaran B, et al. Monocytes enhance the inflammatory response to TLR2 stimulation in aortic valve interstitial cells through paracrine up-regulation of TLR2 level[J]. Int J Biol Sci, 2020, 16(15): 3062-3074. doi: 10.7150/ijbs.49332
[33] Zhang Z, Ge M, Wu D, et al. Resveratrol-loaded sulfated hericium erinaceus β-glucan-chitosan nanoparticles: preparation, characterization and synergistic anti-inflammatory effects[J]. Carbohydr Polym, 2024, 332: 121916. doi: 10.1016/j.carbpol.2024.121916
[34] Chen C, Ma C, Zhang Y, et al. Pioglitazone inhibits advanced glycation end product-induced TNF-α and MMP-13 expression via the antagonism of NF-κB activation in chondrocytes[J]. Pharmacology, 2014, 94(5-6): 265-272. doi: 10.1159/000369074
[35] Garbati MR, Hays LE, Keeble W, et al. FANCA and FANCC modulate TLR and p38 MAPK-dependent expression of IL-1β in macrophages[J]. Blood, 2013, 122(18): 3197-3205. doi: 10.1182/blood-2013-02-484816
[36] Li XF, Yin SQ, Li H, et al. PPAR-γ alleviates the inflammatory response in TNF-α-induced fibroblast-like synoviocytes by binding to p53 in rheumatoid arthritis[J]. Acta Pharmacol Sin, 2023, 44(2): 454-464. doi: 10.1038/s41401-022-00957-9
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