[1]	The WCOTROCHADIC. Report on cardiovascular health and diseases in China 2022:an updated summary[J]. Biomed Environ Sci, 2023, 36(8):669-701.DOI:10.3967/bes2023.106. Cited in this article [1]

[2]

National Center for Cardiovascular Diseases the Writing Committee of the Report on Cardiovascular Health and Diseases in China. Report on cardiovascular health and diseases in China 2023:an updated summary[J]. Biomed Environ Sci, 2024, 37(9):949-992.DOI:10.3967/bes2024.162. Cited in this article [1]

[3]	Zhao D, Liu J, Wang M, et al. Epidemiology of cardiovascular disease in China:current features and implications[J]. Nat Rev Cardiol, 2019, 16(4):203-212.DOI:10.1038/s41569-018-0119-4. Cited in this article [1]

[4]	Libby P. The changing landscape of atherosclerosis[J]. Nature, 2021, 592(7855):524-533.DOI:10.1038/s41586-021-03392-8. Cited in this article [2]

[5]	Zhang J, Xie M, Huang X, et al. The effects of porphyromonas gingivalis on atherosclerosis-related cells[J]. Front Immunol, 2021, 12:766560.DOI:10.3389/fimmu.2021.766560. Cited in this article [1]

[6]	Xu W, Zhou W, Wang H, et al. Roles of porphyromonas gingivalis and its virulence factors in periodontitis[J]. Adv Protein Chem Struct Biol, 2020, 120:45-84.DOI:10.1016/bs.apcsb.2019.12.001. Cited in this article [2]

[7]	Ogawa T, Asai Y, Makimura Y, et al. Chemical structure and immunobiological activity of porphyromonas gingivalis lipid A[J]. Front Biosci, 2007, 12:3795-3812.DOI:10.2741/2353. Cited in this article [1]

[8]	Fitzgerald KA, Kagan JC. Toll-like receptors and the control of immunity[J]. Cell, 2020, 180(6):1044-1066.DOI:10.1016/j.cell.2020.02.041. Cited in this article [1]

[9]	Darveau RP. Periodontitis:a polymicrobial disruption of host homeostasis[J]. Nat Rev Microbiol, 2010, 8(7):481-490. DOI:10.1038/nrmicro2337. Cited in this article [2]

[10]	Olsen I, Hajishengallis G. Major neutrophil functions subverted by porphyromonas gingivalis[J]. J Oral Microbiol, 2016, 8:30936.DOI:10.3402/jom.v8.30936. Cited in this article [1]

[11]	Toyofuku M, Schild S, Kaparakis-Liaskos M, et al. Composition and functions of bacterial membrane vesicles[J]. Nat Rev Microbiol, 2023, 21(7):415-430.DOI:10.1038/s41579-023-00875-5. Cited in this article [1]

[12]	Lunar Silva I, Cascales E. Molecular strategies underlying porphyromonas gingivalis virulence[J]. J Mol Biol, 2021, 433(7):166836.DOI:10.1016/j.jmb.2021.166836. Cited in this article [1]

[13]	Zhang Z, Liu D, Liu S, et al. The role of porphyromonas gingivalis outer membrane vesicles in periodontal disease and related systemic diseases[J]. Front Cell Infect Microbiol, 2021, 10:585917.DOI:10.3389/fcimb.2020.585917. Cited in this article [1]

[14]	Jiao J, Jing W, Si Y, et al. The prevalence and severity of periodontal disease in mainland China:data from the fourth national oral health survey (2015-2016)[J]. J Clin Periodontol, 2021, 48(2):168-179.DOI:10.1111/jcpe.13396. Cited in this article [1]

[15]	Norhammar A, Näsman P, Buhlin K, et al. Does periodontitis increase the risk for future cardiovascular events? Long-term follow-up of the PAROKRANK study[J]. J Clin Periodontol, 2025, 52(1):16-23.DOI:10.1111/jcpe.14064. Cited in this article [1]

[16]	Park JH, Leem GH, Kim JW, et al. Persisting chronic periodontal disease as a risk factor for cardiovascular disease:a nationwide population-based cohort study[J]. J Clin Periodontol, 2025, 52(3):375-386.DOI:10.1111/jcpe.14107. Cited in this article [1]

[17]	Kanpittaya B, Lertpimonchai A, Mongkornkarn S, et al. Periodontitis is associated with arterial stiffness as measured by serial cardio-ankle vascular index (CAVI):a 10-year cohort study[J]. J Clin Periodontol, 2025, 52(3):363-374.DOI:10.1111/jcpe.14086. Cited in this article [1]

[18]	Teeuw WJ, Slot DE, Susanto H, et al. Treatment of periodontitis improves the atherosclerotic profile:a systematic review and meta-analysis[J]. J Clin Periodontol, 2014, 41(1):70-79. DOI:10.1111/jcpe.12171. Cited in this article [1]

[19]	Socransky SS, Haffajee AD, Cugini MA, et al. Microbial complexes in subgingival plaque[J]. J Clin Periodontol, 1998, 25(2):134-144.DOI:10.1111/j.1600-051x.1998.tb02419.x. Cited in this article [1]

[20]	Bravo-Lopez M, Villa-Islas V, Rocha Arriaga C, et al. Paleogenomic insights into the red complex bacteria tannerella forsythia in pre-hispanic and colonial individuals from Mexico[J]. Philos Trans R Soc Lond B Biol Sci, 2020, 375(1812):20190580.DOI:10.1098/rstb.2019.0580. Cited in this article [1]

[21]

Jepsen K, Falk W, Brune F, et al. Prevalence and antibiotic susceptibility trends of periodontal pathogens in the subgingival microbiota of German periodontitis patients:a retrospective surveillance study[J]. J Clin Periodontol, 2021, 48(9):1216-1227.DOI:10.1111/jcpe.13468. Cited in this article [1]

[22]	Beck JD, Eke P, Lin D, et al. Associations between IgG antibody to oral organisms and carotid intima-medial thickness in community-dwelling adults[J]. Atherosclerosis, 2005, 183(2):342-348.DOI:10.1016/j.atherosclerosis.2005.03.017. Cited in this article [1]

[23]	Van den Munckhof ICL, Jones H, Hopman MTE, et al. Relation between age and carotid artery intima-medial thickness:a systematic review[J]. Clin Cardiol, 2018, 41(5):698-704. DOI:10.1002/clc.22934. Cited in this article [1]

[24]	Pavlic V, Peric D, Kalezic IS, et al. Identification of periopathogens in atheromatous plaques obtained from carotid and coronary arteries[J]. Biomed Res Int, 2021, 2021:9986375. DOI:10.1155/2021/9986375. Cited in this article [1]

[25]	Immanuel J, Yun S. Vascular inflammatory diseases and endothelial phenotypes[J]. Cells, 2023, 12(12):1640.DOI:10.3390/cells12121640. Cited in this article [1]

[26]	Vijay K. Toll-like receptors in immunity and inflammatory diseases:past,present,and future[J]. Int Immunopharmacol, 2018, 59:391-412.DOI:10.1016/j.intimp.2018.03.002. Cited in this article [1]

[27]	Jin M, Fang J, Wang JJ, et al. Regulation of toll-like receptor (TLR) signaling pathways in atherosclerosis:from mechanisms to targeted therapeutics[J]. Acta Pharmacol Sin, 2023, 44(12):2358-2375.DOI:10.1038/s41401-023-01123-5. Cited in this article [1]

[28]

Chukkapalli SS, Ambadapadi S, Varkoly K, et al. Impaired innate immune signaling due to combined Toll-like receptor 2 and 4 deficiency affects both periodontitis and atherosclerosis in response to polybacterial infection[J]. Pathog Dis, 2018, 76(8):fty076.DOI:10.1093/femspd/fty076. Cited in this article [1]

[29]	Inaba H, Yoshida S, Nomura R, et al. Porphyromonas gulae lipopolysaccharide elicits inflammatory responses through Toll-like receptor 2 and 4 in human gingivalis epithelial cells[J]. Cell Microbiol, 2020, 22(12):e13254.DOI:10.1111/cmi.13254. Cited in this article [1]

[30]	Groeger S, Jarzina F, Domann E, et al. Porphyromonas gingivalis activates NF-κB and MAPK pathways in human oral epithelial cells[J]. BMC Immunol, 2017, 18(1):1.DOI:10.1186/s12865-016-0185-5. Cited in this article [1]

[31]	Xie M, Tang Q, Yu S, et al. Porphyromonas gingivalis disrupts vascular endothelial homeostasis in a TLR-NF-κB axis dependent manner[J]. Int J Oral Sci, 2020, 12(1):28.DOI:10.1038/s41368-020-00096-z. Cited in this article [2]

[32]	Aleksijević LH, Aleksijević M, Škrlec I, et al. Porphyromonas gingivalis virulence factors and cinical significance in periodontal disease and coronary artery diseases[J]. Pathogens, 2022, 11(10):1173.DOI:10.3390/pathogens11101173. Cited in this article [1]

[33]	Kawai T, Akira S. Signaling to NF-κB by Toll-like receptors[J]. Trends Mol Med, 2007, 13(11):460-469.DOI:10.1016/j.molmed.2007.09.002. Cited in this article [2]

[34]	Brown J, Wang H, Hajishengallis GN, et al. TLR-signaling networks:an integration of adaptor molecules,kinases,and cross-talk[J]. J Dent Res, 2011, 90(4):417-427.DOI:10.1177/0022034510381264. Cited in this article [1]

[35]	Xie M, Tang Q, Nie J, et al. BMAL1-downregulation aggravates porphyromonas gingivalis-induced atherosclerosis by encouraging oxidative stress[J]. Circ Res, 2020, 126(6):e15-e29.DOI:10.1161/circresaha.119.315502. Cited in this article [2]

[36]	Tang YS, Zhao YH, Zhong Y, et al. Neferine inhibits LPS-ATP-induced endothelial cell pyroptosis via regulation of ROS/NLRP3/caspase-1 signaling pathway[J]. Inflamm Res, 2019, 68(9):727-738.DOI:10.1007/s00011-019-01256-6. Cited in this article [2]

[37]

Chen Q, Guo C, Zhou X, et al. N-acetylneuraminic acid and chondroitin sulfate modified nanomicelles with ROS-sensitive H2S donor via targeting E-selectin receptor and CD44 receptor for the efficient therapy of atherosclerosis[J]. Int J Biol Macromol, 2022, 211:259-270.DOI:10.1016/j.ijbiomac.2022.04.180. Cited in this article [1]

[38]	Kobayashi N, Suzuki JI, Aoyama N, et al. Toll-like receptor 4 signaling has a critical role in porphyromonas gingivalis-accelerated neointimal formation after arterial injury in mice[J]. Hypertens Res, 2016, 39(10):717-722.DOI:10.1038/hr.2016.58. Cited in this article [1]

[39]

Nakamura N, Yoshida M, Umeda M, et al. Extended exposure of lipopolysaccharide fraction from porphyromonas gingivalis facilitates mononuclear cell adhesion to vascular endothelium via Toll-like receptor-2 dependent mechanism[J]. Atherosclerosis, 2008, 196(1):59-67.DOI:10.1016/j.atherosclerosis.2007.01.039. Cited in this article [1]

[40]	Andrukhov O, Steiner I, Liu S, et al. Different effects of porphyromonas gingivalis lipopolysaccharide and TLR2 agonist Pam3CSK4 on the adhesion molecules expression in endothelial cells[J]. Odontology, 2015, 103(1):19-26.DOI:10.1007/s10266-013-0146-x. Cited in this article [1]

[41]	Hayashi C, Papadopoulos G, Gudino CV, et al. Protective role for TLR4 signaling in atherosclerosis progression as revealed by infection with a common oral pathogen[J]. J Immunol, 2012, 189(7):3681-3688.DOI:10.4049/jimmunol.1201541. Cited in this article [1]

[42]	Chistiakov DA, Melnichenko AA, Myasoedova VA, et al. Mechanisms of foam cell formation in atherosclerosis[J]. J Mol Med (Berl), 2017, 95(11):1153-1165.DOI:10.1007/s00109-017-1575-8. Cited in this article [2]

[43]	Fernández-Ruiz I. Macropinocytosis promotes foam cell formation and atherosclerosis[J]. Nat Rev Cardiol, 2022, 19(12):781.DOI:10.1038/s41569-022-00798-3. Cited in this article [1]

[44]	Pryma CS, Ortega C, Dubland JA, et al. Pathways of smooth muscle foam cell formation in atherosclerosis[J]. Curr Opin Lipidol, 2019, 30(2):117-124.DOI:10.1097/mol.0000000000000574. Cited in this article [2]

[45]	Kawai T, Akira S. TLR signaling[J]. Semin Immunol, 2007, 19(1):24-32.DOI:10.1016/j.smim.2006.12.004. Cited in this article [1]

[46]	Huang Y, Tian C, Li Q, et al. TET1 knockdown inhibits porphyromonas gingivalis LPS/IFN-γ-induced M1 macrophage polarization through the NF-κB pathway in THP-1 cells[J]. Int J Mol Sci, 2019, 20(8):2023.DOI:10.3390/ijms20082023. Cited in this article [1]

[47]	Afzoon S, Amiri MA, Mohebbi M, et al. A systematic review of the impact of porphyromonas gingivalis on foam cell formation:implications for the role of periodontitis in atherosclerosis[J]. BMC Oral Health, 2023, 23(1):481.DOI:10.1186/s12903-023-03183-9. Cited in this article [1]

[48]	Tian K, Xu Y, Sahebkar A, et al. CD36 in atherosclerosis:pathophysiological mechanisms and therapeutic implications[J]. Curr Atheroscler Rep, 2020, 22(10):59.DOI:10.1007/s11883-020-00870-8. Cited in this article [1]

[49]	Huck O, Elkaim R, Davideau JL, et al. Porphyromonas gingivalis-impaired innate immune response via NLRP3 proteolysis in endothelial cells[J]. Innate Immun, 2015, 21(1):65-72. DOI:10.1177/1753425914523459. Cited in this article [1]

[50]	Echeverría C, Montorfano I, Tapia P, et al. Endotoxin-induced endothelial fibrosis is dependent on expression of transforming growth factors β1 and β2[J]. Infect Immun, 2014, 82(9):3678-3686.DOI:10.1128/iai.02158-14. Cited in this article [1]

[51]	Maekawa T, Tabeta K, Kajita-Okui K, et al. Increased expression of C-reactive protein gene in inflamed gingival tissues could be derived from endothelial cells stimulated with interleukin-6[J]. Arch Oral Biol, 2011, 56(11):1312-1318.DOI:10.1016/j.archoralbio.2011.04.010. Cited in this article [1]

[52]	Suh JS, Kim S, Boström KI, et al. Periodontitis-induced systemic inflammation exacerbates atherosclerosis partly via endothelial-mesenchymal transition in mice[J]. Int J Oral Sci, 2019, 11(3):21.DOI:10.1038/s41368-019-0054-1. Cited in this article [1]

[53]	Pollreisz A, Huang Y, Roth GA, et al. Enhanced monocyte migration and pro-inflammatory cytokine production by porphyromonas gingivalis infection[J]. J Periodontal Res, 2010, 45(2):239-245.DOI:10.1111/j.1600-0765.2009.01225.x. Cited in this article [1]

[54]	Lei L, Li H, Yan F, et al. Porphyromonas gingivalis lipopolysaccharide alters atherosclerotic-related gene expression in oxidized low-density-lipoprotein-induced macrophages and foam cells[J]. J Periodontal Res, 2011, 46(4):427-437.DOI:10.1111/j.1600-0765.2011.01356.x. Cited in this article [1]

[55]	Capece D, Verzella D, Flati I, et al. NF-κB:blending metabolism,immunity,and inflammation[J]. Trends Immunol, 2022, 43(9):757-775.DOI:10.1016/j.it.2022.07.004. Cited in this article [1]

[56]	Hoseini Z, Sepahvand F, Rashidi B, et al. NLRP3 inflammasome:its regulation and involvement in atherosclerosis[J]. J Cell Physiol, 2018, 233(3):2116-2132.DOI:10.1002/jcp.25930. Cited in this article [1]

[57]	Nie R, Wu Z, Ni J, et al. Porphyromonas gingivalis infection induces amyloid-β accumulation in monocytes/macrophages[J]. J Alzheimers Dis, 2019, 72(2):479-494.DOI:10.3233/jad-190298. Cited in this article [1]

[58]	Grebe A, Hoss F, Latz E. NLRP3 inflammasome and the IL-1 pathway in atherosclerosis[J]. Circ Res, 2018, 122(12):1722-1740.DOI:10.1161/circresaha.118.311362. Cited in this article [1]

[59]	Li C, Yin W, Yu N, et al. MiR-155 promotes macrophage pyroptosis induced by porphyromonas gingivalis through regulating the NLRP3 inflammasome[J]. Oral Dis, 2019, 25(8):2030-2039.DOI:10.1111/odi.13198. Cited in this article [1]

[60]	Castro SA, Collighan R, Lambert PA, et al. Porphyromonas gingivalis gingipains cause defective macrophage migration towards apoptotic cells and inhibit phagocytosis of primary apoptotic neutrophils[J]. Cell Death Dis, 2017, 8(3):e2644. DOI:10.1038/cddis.2016.481. Cited in this article [1]

[61]	Bennett MR, Sinha S, Owens GK. Vascular smooth muscle cells in atherosclerosis[J]. Circ Res, 2016, 118(4):692-702. DOI:10.1161/circresaha.115.306361. Cited in this article [1]

[62]	Miyabe M, Nakamura N, Saiki T, et al. Porphyromonas gingivalis lipopolysaccharides promote proliferation and migration of human vascular smooth muscle cells through the MAPK/TLR4 pathway[J]. Int J Mol Sci, 2022, 24(1):125.DOI:10.3390/ijms24010125. Cited in this article [1]

[63]	Kim Y, Kim SJ, Bae MK, et al. Porphyromonas gingivalis lipopolysaccharide regulates migration of vascular smooth muscle cells[J]. Int J Oral Biol, 2016, 41(4):217-223.DOI:10.11620/IJOB.2016.41.4.217. Cited in this article [1]

[64]	Bugueno IM, Khelif Y, Seelam N, et al. Porphyromonas gingivalis differentially modulates cell death profile in ox-LDL and TNF-α pre-treated endothelial cells[J]. PLoS One, 2016, 11(4):e0154590.DOI10.1371/journal.pone.0154590. Cited in this article [1]

[65]	Rao A, Kumar BK. Role of periodontal pathogens in atherosclerotic plaque development and progression:an overview[J]. Acta Microbiol Immunol Hung, 2023, 70(4):272-277.DOI:10.1556/030.2023.02145. Cited in this article [1]

[66]	Thakare KS, Deo V, Bhongade ML. Evaluation of the C-reactive protein serum levels in periodontitis patients with or without atherosclerosis[J]. Indian J Dent Res, 2010, 21(3):326-329.DOI:10.4103/0970-9290.70787. Cited in this article [1]

[67]	Lin G, Shi X, Chen S, et al. Effects of micro-amounts of porphyromonas gingivalis lipopolysaccharide on rabbit inflammatory immune response and development of atherosclerosis[J]. J Periodontal Res, 2015, 50(3):356-362.DOI:10.1111/jre.12214. Cited in this article [1]

[68]	Ruan Q, Guan P, Qi W, et al. Porphyromonas gingivalis regulates atherosclerosis through an immune pathway[J]. Front Immunol, 2023, 14:1103592.DOI:10.3389/fimmu.2023.1103592. Cited in this article [1]

[69]	He X, Liang B, Gu N. Th17/Treg imbalance and atherosclerosis[J]. Dis Markers, 2020, 2020:8821029.DOI:10.1155/2020/8821029. Cited in this article [1]

[70]	Li Y, Gu Y, Yang P, et al. CD69 is a promising immunotherapy and prognosis prediction target in cancer[J]. Immunotargets Ther, 2024, 13:1-14.DOI:10.2147/itt.S439969. Cited in this article [1]

[71]	Wang Y, Zhang W, Xu L, et al. Porphyromonas gingivalis lipopolysaccharide induced proliferation and activation of natural killer cells in vivo[J].Molecules, 2016, 21(8):1086. DOI:10.3390/molecules21081086. Cited in this article [1]

[72]	Tsilingiri K, de la Fuente H, Relaño M, et al. Oxidized low-density lipoprotein receptor in lymphocytes prevents atherosclerosis and predicts subclinical disease[J]. Circulation, 2019, 139(2):243-255.DOI:10.1161/circulationaha.118.034326. Cited in this article [1]

[73]	Yang J, Wu J, Zhang R, et al. Porphyromonas gingivalis oral infection promote T helper 17/Treg imbalance in the development of atherosclerosis[J]. J Dent Sci, 2017, 12(1):60-69.DOI:10.1016/j.jds.2016.10.003. Cited in this article [1]

[74]	Viafara-García SM, Morantes SJ, Chacon-Quintero Y, et al. Repeated porphyromonas gingivalis W83 exposure leads to release pro-inflammatory cytokynes and angiotensin Ⅱ in coronary artery endothelial cells[J]. Sci Rep, 2019, 9(1):19379.DOI:10.1038/s41598-019-54259-y. Cited in this article [1]

[75]	He TR, Tang XY, Yan Q, et al. All-trans retinoic acid-incorporated glycol chitosan nanoparticles regulate macrophage polarization in Pg-LPS-induced inflammation[J]. Curr Med Sci, 2022, 42(5):974-980.DOI:10.1007/s11596-022-2602-8. Cited in this article [1]

[76]	Xie H, Qin Z, Ling Z, et al. Oral pathogen aggravates atherosclerosis by inducing smooth muscle cell apoptosis and repressing macrophage efferocytosis[J]. Int J Oral Sci, 2023, 15(1):26.DOI:10.1038/s41368-023-00232-5. Cited in this article [1]

[77]	Yan N, Xu J, Liu G, et al. Penetrating macrophage-based nanoformulation for periodontitis treatment[J]. ACS Nano, 2022, 16(11):18253-18265.DOI:10.1021/acsnano.2c05923. Cited in this article [1]

[78]	Tekce M, Ince G, Gursoy H, et al. Clinical and microbiological effects of probiotic lozenges in the treatment of chronic periodontitis:a 1-year follow-up study[J]. J Clin Periodontol, 2015, 42(4):363-372.DOI:10.1111/jcpe.12387. Cited in this article [2]

[79]	Jia B, Zou Y, Han X, et al. Gut microbiome-mediated mechanisms for reducing cholesterol levels:implications for ameliorating cardiovascular disease[J]. Trends Microbiol, 2023, 31(1):76-91.DOI:10.1016/j.tim.2022.08.003. Cited in this article [1]

[80]	Scannapieco FA, Gershovich E. The prevention of periodontal disease-an overview[J]. Periodontol, 2020, 84(1):9-13. DOI:10.1111/prd.12330. Cited in this article [1]

[81]	Tang J, Li T, Xiong X, et al. Colchicine delivered by a novel nanoparticle platform alleviates atherosclerosis by targeted inhibition of NF-κB/NLRP3 pathways in inflammatory endothelial cells[J]. J Nanobiotechnology, 2023, 21(1):460. DOI:10.1186/s12951-023-02228-z. Cited in this article [1]

[82]	Zhu Y, Fang Y, Wang Y, et al. Cluster of differentiation-44-targeting prussian blue nanoparticles onloaded with colchicine for atherosclerotic plaque regression in a mice model[J]. ACS Biomater Sci Eng, 2024, 10(3):1530-1543.DOI:10.1021/acsbiomaterials.3c01518. Cited in this article [1]

[83]

Herrera D, Sanz M, Shapira L, et al. Association between periodontal diseases and cardiovascular diseases,diabetes and respiratory diseases:consensus report of the Joint Workshop by the European Federation of Periodontology (EFP) and the European arm of the World Organization of Family Doctors (WONCA Europe)[J]. J Clin Periodontol, 2023, 50(6):819-841.DOI:10.1111/jcpe.13807. Cited in this article [2]

[84]	Orlandi M, Muñoz Aguilera E, Marletta D, et al. Impact of the treatment of periodontitis on systemic health and quality of life:a systematic review[J]. J Clin Periodontol, 2022, 49(Suppl 24):314-327.DOI:10.1111/jcpe.13554. Cited in this article [1]

[85]	Herrera D, Molina A, Buhlin K, et al. Periodontal diseases and association with atherosclerotic disease[J]. Periodontol 2000, 2020, 83(1):66-89.DOI:10.1111/prd.12302. Cited in this article [1]