[1] [1] Kuriakose D, Xiao Z. Pathophysiology and treatment of stroke: present status and future perspectives[J]. Int J Mol Sci, 2020, 21(20):7609.

[2] [2] Vivien D. New opportunities for diagnosis and prognosis of stroke: the benefits of across border approaches[J]. Hamostaseologie, 2021, 41(1):22-24.

[3] [3] Zhao Y, Zhang X, Chen X, et al. Neuronal injuries in cerebral infarction and ischemic stroke: From mechanisms to treatment (Review) [J]. Int J Mol Med, 2022, 49(2):15.

[4] [4] Feigin VL, Brainin M, Norrving B, et al. World Stroke Organization (WSO): global stroke fact sheet 2022[J]. Int J Stroke, 2022, 17(1):18-29.

[5] [5] Tu WJ, Wang LD. China stroke surveillance report 2021[J]. Mil Med Res, 2023, 10(1):33.

[6] [6] Sills GJ, Rogawski MA. Mechanisms of action of currently used antiseizure drugs[J]. Neuropharmacology, 2020, 168:107966.

[7] [7] Patejdl R, Leroux AC, Noack T. Phenytoin inhibits contractions of rat gastrointestinal and portal vein smooth muscle by inhibiting calcium entry[J]. Neurogastroenterol Motil, 2015, 27(10):1453-1465.

[8] [8] Candeloro M, Eikelboom JW, Chan N, et al. Carbamazepine, phenytoin, and oral anticoagulants: Drug-drug interaction and clinical events in a retrospective cohort[J]. Res Pract Thromb Haemost, 2022, 6(2):e12650.

[9] [9] Tani S, Shimizu T, Kasuya H, et al. Induction of cerebral thrombosis with phenytoin in rats[J]. Stroke, 1995, 26(11):2081-2086.

[10] [10] Birney E. Mendelian randomization[J]. Cold Spring Harb Perspect Med, 2022, 12(4):a041302.

[11] [11] Jiang L, Zheng Z, Fang H, et al. A generalized linear mixed model association tool for biobank-scale data[J]. Nat Genet, 2021, 53(11):1616-1621.

[12] [12] Malik R, Chauhan G, Traylor M, et al. Multiancestry genome-wide association study of 520,000 subjects identifies 32 loci associated with stroke and stroke subtypes[J]. Nat Genet, 2018, 50(4):524-537.

[13] [13] Sakaue S, Kanai M, Tanigawa Y, et al. A cross-population atlas of genetic associations for 220 human phenotypes[J]. Nat Genet, 2021, 53(10):1415-1424.

[14] [14] Traylor M, Persyn E, Tomppo L, et al. Genetic basis of lacunar stroke: a pooled analysis of individual patient data and genome-wide association studies[J]. Lancet Neurol, 2021, 20(5):351-361.

[15] [15] Li P, Wang H, Guo L, et al. Association between gut microbiota and preeclampsia-eclampsia: a two-sample Mendelian randomization study[J]. BMC Med, 2022, 20(1):443.

[16] [16] Sanna S, Van Zuydam NR, Mahajan A, et al. Causal relationships among the gut microbiome, short-chain fatty acids and metabolic diseases[J]. Nat Genet, 2019, 51(4):600-605.

[18] [18] Pierce BL, Ahsan H, Vanderweele TJ. Power and instrument strength requirements for Mendelian randomization studies using multiple genetic variants[J]. Int J Epidemiol, 2011, 40(3):740-752.

[19] [19] Bowden J, Holmes MV. Meta-analysis and Mendelian randomization: A review[J]. Res Synth Methods, 2019, 10(4):486-496.

[20] [20] Zhao J, Ming J, Hu X, et al. Bayesian weighted Mendelian randomization for causal inference based on summary statistics[J]. Bioinformatics, 2020, 36(5):1501-1508.

[21] [21] Shen Y, Liu H, Meng X, et al. The causal effects between gut microbiota and hemorrhagic stroke: a bidirectional two-sample Mendelian randomization study[J]. Front Microbiol, 2023, 14:1290909.

[22] [22] Burgess S, Thompson SG. Interpreting findings from Mendelian randomization using the MR-Egger method [J]. Eur J Epidemiol, 2017, 32(5):377-389.

[23] [23] Xu J, Zhang S, Tian Y, et al. Genetic causal association between iron status and osteoarthritis: a two-sample Mendelian randomization[J]. Nutrients, 2022, 14(18):3683.

[24] [24] Chen X, Hong X, Gao W, et al. Causal relationship between physical activity, leisure sedentary behaviors and COVID-19 risk: a Mendelian randomization study[J]. J Transl Med, 2022, 20(1):216.

[25] [25] Vega-Riquer JM, Campos-Ordonez T, Galvez-Contreras AY, et al. Phenytoin promotes the proliferation of oligodendrocytes and enhances the expression of myelin basic protein in the corpus callosum of mice demyelinated by cuprizone[J]. Exp Brain Res, 2022, 240(5):1617-1627.

[26] [26] LaRoche SM, Helmers SL. The new antiepileptic drugs: scientific review[J]. JAMA, 2004, 291(5):605-614.

[27] [27] Komider K, Kamieniak M, Czuczwar SJ, et al. Second generation of antiepileptic drugs and oxidative stress[J]. Int J Mol Sci, 2023, 24(4):3873.

[28] [28] Rocha NP, Assis F, Scalzo PL, et al. Reduced activated T lymphocytes (CD4+CD25+) and plasma levels of cytokines in Parkinson's disease[J]. Mol Neurobiol, 2018, 55(2):1488-1497.

[29] [29] Johnson AG, Nguyen TV, Day RO. Do nonsteroidal anti-inflammatory drugs affect blood pressure? A meta-analysis[J]. Ann Intern Med, 1994, 121(4):289-300.

[30] [30] Johnson AG. NSAIDs and increased blood pressure. What is the clinical significance[J]? Drug Saf, 1997, 17(5):277-289.

[31] [31] Majesky MW, Weiser-Evans MCM. The adventitia in arterial development, remodeling, and hypertension[J]. Biochem Pharmacol, 2022, 205:115259.

[32] [32] Hu H, Garcia-Barrio M, Jiang ZS, et al. Roles of perivascular adipose tissue in hypertension and atherosclerosis[J]. Antioxid Redox Signal, 2021, 34(9):736-749.

[33] [33] Heistad DD, Lopez JA, Baumbach GL. Hemodynamic determinants of vascular changes in hypertension and atherosclerosis[J]. Hypertension, 1991, 17(4 Suppl):III7-11.