[1] Costantino S, Paneni F, Cosentino F. Ageing, metabolism and cardiovascular disease. J Physiol, 2016; 594, 2061−73. doi:  10.1113/JP270538
[2] Hou YJ, Dan XL, Babbar M, et al. Ageing as a risk factor for neurodegenerative disease. Nat Rev Neurol, 2019; 15, 565−81. doi:  10.1038/s41582-019-0244-7
[3] North BJ, Sinclair DA. The intersection between aging and cardiovascular disease. Circ Res, 2012; 110, 1097−108. doi:  10.1161/CIRCRESAHA.111.246876
[4] Ungvari Z, Tarantini S, Donato AJ, et al. Mechanisms of vascular aging. Circ Res, 2018; 123, 849−67. doi:  10.1161/CIRCRESAHA.118.311378
[5] Seals DR, Alexander LM. Vascular aging. J Appl Physiol (1985), 2018; 125, 1841−2. doi:  10.1152/japplphysiol.00448.2018
[6] Thijssen DHJ, Carter SE, Green DJ. Arterial structure and function in vascular ageing: are you as old as your arteries?. J Physiol, 2016; 594, 2275−84. doi:  10.1113/JP270597
[7] Cao QD, Wu JP, Wang XL, et al. Noncoding RNAs in vascular aging. Oxid Med Cell Longev, 2020; 2020, 7914957.
[8] Guzik TJ, Touyz RM. Oxidative stress, inflammation, and vascular aging in hypertension. Hypertension, 2017; 70, 660−7. doi:  10.1161/HYPERTENSIONAHA.117.07802
[9] Wang MY, Kim SH, Monticone RE, et al. Matrix metalloproteinases promote arterial remodeling in aging, hypertension, and atherosclerosis. Hypertension, 2015; 65, 698−703. doi:  10.1161/HYPERTENSIONAHA.114.03618
[10] Barallobre-Barreiro J, Loeys B, Mayr M, et al. Extracellular matrix in vascular disease, part 2/4: JACC focus seminar. J Am Coll Cardiol, 2020; 75, 2189−203.
[11] Cheng XW, Kuzuya M, Nakamura K, et al. Mechanisms underlying the impairment of ischemia-induced neovascularization in matrix metalloproteinase 2–deficient mice. Circ Res, 2007; 100, 904−13. doi:  10.1161/01.RES.0000260801.12916.b5
[12] Vigetti D, Moretto P, Viola M, et al. Matrix metalloproteinase 2 and tissue inhibitors of metalloproteinases regulate human aortic smooth muscle cell migration during in vitro aging. FASEB J, 2006; 20, 1118−30. doi:  10.1096/fj.05-4504com
[13] Wang MY, Monticone RE, McGraw KR. Proinflammation, profibrosis, and arterial aging. Aging Med, 2020; 3, 159−68. doi:  10.1002/agm2.12099
[14] Spiers JP, Kelso EJ, Siah WF, et al. Alterations in vascular matrix metalloproteinase due to ageing and chronic hypertension: effects of endothelin receptor blockade. J Hypertens, 2005; 23, 1717−24. doi:  10.1097/01.hjh.0000176787.04753.ee
[15] Piao LM, Zhao GX, Zhu EB, et al. Chronic psychological stress accelerates vascular senescence and impairs ischemia‐induced neovascularization: the role of dipeptidyl peptidase‐4/glucagon‐like peptide‐1‐adiponectin axis. J Am Heart Assoc, 2017; 6, e006421. doi:  10.1161/JAHA.117.006421
[16] Xu SN, Piao LM, Wan Y, et al. CTSS modulates stress-related carotid artery thrombosis in a mouse FeCl3 model. Arterioscler Thromb Vasc Biol, 2023; 43, e238−53.
[17] Lei YN, Yang G, Hu LN, et al. Increased dipeptidyl peptidase-4 accelerates diet-related vascular aging and atherosclerosis in ApoE-deficient mice under chronic stress. Int J Cardiol, 2017; 243, 413−20. doi:  10.1016/j.ijcard.2017.05.062
[18] Kim S, Misra A. SNP genotyping: technologies and biomedical applications. Annu Rev Biomed Eng, 2007; 9, 289−320. doi:  10.1146/annurev.bioeng.9.060906.152037
[19] Shimizu S, Mimura J, Hasegawa T, et al. Association of single nucleotide polymorphisms in the NRF2 promoter with vascular stiffness with aging. PLoS One, 2020; 15, e0236834. doi:  10.1371/journal.pone.0236834
[20] Liao YC, Liu PY, Lin HF, et al. Two functional polymorphisms of ROCK2 enhance arterial stiffening through inhibiting its activity and expression. J Mol Cell Cardiol, 2015; 79, 180−6. doi:  10.1016/j.yjmcc.2014.11.023
[21] Vlachopoulos C, Xaplanteris P, Baou K, et al. Common single nucleotide polymorphisms of the p22phox NADPH oxidase subunit do not influence aortic stiffness in young, healthy adults. Hellenic J Cardiol, 2012; 53, 352−6.
[22] Cunha PG, Boutouyrie P, Nilsson PM, et al. Early vascular ageing (EVA): definitions and clinical applicability. Curr Hypertens Rev, 2017; 13, 8−15.
[23] The Reference Values for Arterial Stiffness’ Collaboration. Determinants of pulse wave velocity in healthy people and in the presence of cardiovascular risk factors: ‘establishing normal and reference values’. Eur Heart J, 2010; 31, 2338−50. doi:  10.1093/eurheartj/ehq165
[24] He H, Deng Y, Wan H, et al. Urinary bisphenol A and its interaction with CYP17A1 rs743572 are associated with breast cancer risk. Chemosphere, 2022; 286, 131880. doi:  10.1016/j.chemosphere.2021.131880
[25] Cabral-Pacheco GA, Garza-Veloz I, Castruita-De La Rosa C, et al. The roles of matrix metalloproteinases and their inhibitors in human diseases. Int J Mol Sci, 2020; 21, 9739. doi:  10.3390/ijms21249739
[26] Perrocheau M, Kiando SR, Vernerey D, et al. Investigation of the matrix metalloproteinase-2 gene in patients with non-syndromic mitral valve prolapse. J Cardiovasc Dev Dis, 2015; 2, 176−89.
[27] Basalyga DM, Simionescu DT, Xiong WF, et al. Elastin degradation and calcification in an abdominal aorta injury model: role of matrix metalloproteinases. Circulation, 2004; 110, 3480−7. doi:  10.1161/01.CIR.0000148367.08413.E9
[28] Thompson M, Cockerill G. Matrix metalloproteinase-2: the forgotten enzyme in aneurysm pathogenesis. Ann N Y Acad Sci, 2006; 1085, 170−4. doi:  10.1196/annals.1383.034
[29] Qi FR, Liu Y, Zhang KL, et al. Artificial intelligence uncovers natural MMP inhibitor crocin as a potential treatment of thoracic aortic aneurysm and dissection. Front Cardiovasc Med, 2022; 9, 871486. doi:  10.3389/fcvm.2022.871486
[30] Zehtabi F, Ispas-Szabo P, Djerir D, et al. Chitosan-doxycycline hydrogel: an MMP inhibitor/sclerosing embolizing agent as a new approach to endoleak prevention and treatment after endovascular aneurysm repair. Acta Biomater, 2017; 64, 94−105. doi:  10.1016/j.actbio.2017.09.021
[31] Kroon AM, Taanman JW. Clonal expansion of T cells in abdominal aortic aneurysm: a role for doxycycline as drug of choice? Int J Mol Sci, 2015; 16, 11178-95.
[32] Elahirad S, Elieh Ali Komi D, Kiani A, et al. Association of matrix metalloproteinase-2 (MMP-2) and MMP-9 promoter polymorphisms, their serum levels, and activities with coronary artery calcification (CAC) in an Iranian population. Cardiovasc Toxicol, 2022; 22, 118−29. doi:  10.1007/s12012-021-09707-5
[33] Alg VS, Ke XY, Grieve J, et al. Association of functional MMP-2 gene variant with intracranial aneurysms: case-control genetic association study and meta-analysis. Br J Neurosurg, 2018; 32, 255−9. doi:  10.1080/02688697.2018.1427213
[34] Wu WX, Liu DY, Jiang SL, et al. Polymorphisms in gene MMP-2 modify the association of cadmium exposure with hypertension risk. Environ Int, 2019; 124, 441−7. doi:  10.1016/j.envint.2019.01.041
[35] Wang N, Zhou S, Fang XC, et al. MMP-2, -3 and TIMP-2, -3 polymorphisms in colorectal cancer in a Chinese Han population: a case-control study. Gene, 2020; 730, 144320. doi:  10.1016/j.gene.2019.144320
[36] Tsai EM, Wang YS, Lin CS, et al. A microRNA-520 mirSNP at the MMP2 gene influences susceptibility to endometriosis in Chinese women. J Hum Genet, 2013; 58, 202−9. doi:  10.1038/jhg.2013.1
[37] Fatar M, Stroick M, Steffens M, et al. Single-nucleotide polymorphisms of MMP-2 gene in stroke subtypes. Cerebrovasc Dis, 2008; 26, 113−9. doi:  10.1159/000139657
[38] Deshmane SL, Kremlev S, Amini S, et al. Monocyte chemoattractant protein-1 (MCP-1): an overview. J Interferon Cytokine Res, 2009; 29, 313−26. doi:  10.1089/jir.2008.0027
[39] Zhu SP, Liu M, Bennett S, et al. The molecular structure and role of CCL2 (MCP‐1) and C‐C chemokine receptor CCR2 in skeletal biology and diseases. J Cell Physiol, 2021; 236, 7211−22. doi:  10.1002/jcp.30375
[40] Singh S, Anshita D, Ravichandiran V. MCP-1: function, regulation, and involvement in disease. Int Immunopharmacol, 2021; 101, 107598. doi:  10.1016/j.intimp.2021.107598
[41] Wang MY, Spinetti G, Monticone RE, et al. A local proinflammatory signalling loop facilitates adverse age-associated arterial remodeling. PLoS One, 2011; 6, e16653. doi:  10.1371/journal.pone.0016653
[42] Zhang HX, Yang K, Chen F, et al. Role of the CCL2-CCR2 axis in cardiovascular disease: pathogenesis and clinical implications. Front Immunol, 2022; 13, 975367. doi:  10.3389/fimmu.2022.975367
[43] Guo X, Cai DP, Dong K, et al. DOCK2 deficiency attenuates abdominal aortic aneurysm formation—brief report. Arterioscler Thromb Vasc Biol, 2023; 43, e210−7.
[44] Brenner D, Labreuche J, Touboul PJ, et al. Cytokine polymorphisms associated with carotid intima-media thickness in stroke patients. Stroke, 2006; 37, 1691−6. doi:  10.1161/01.STR.0000226565.76113.6c
[45] Jemaa R, Rojbani H, Kallel A, et al. Association between the −2518G/A polymorphism in the monocyte chemoattractant protein-1 (MCP-1) gene and myocardial infarction in Tunisian patients. Clin Chim Acta, 2008; 390, 122−5. doi:  10.1016/j.cca.2008.01.004
[46] Xu ZH, Li J, Yang HY, et al. Association of CCL2 gene variants with osteoarthritis. Arch Med Res, 2019; 50, 86−90. doi:  10.1016/j.arcmed.2019.05.014
[47] Feng WX, Mokrousov I, Wang BB, et al. Tag SNP polymorphism of CCL2 and its role in clinical tuberculosis in Han Chinese pediatric population. PLoS One, 2011; 6, e14652. doi:  10.1371/journal.pone.0014652
[48] Motsinger AA, Ritchie MD. Multifactor dimensionality reduction: an analysis strategy for modelling and detecting gene - gene interactions in human genetics and pharmacogenomics studies. Hum Genomics, 2006; 2, 318. doi:  10.1186/1479-7364-2-5-318