口腔微生物组在动脉粥样硬化性心血管疾病中的研究进展

阚九旭, 闫薇, 高云龙, 等. 口腔微生物组在动脉粥样硬化性心血管疾病中的研究进展[J]. 临床心血管病杂志, 2024, 40(6): 453-456. doi: 10.13201/j.issn.1001-1439.2024.06.006
引用本文: 阚九旭, 闫薇, 高云龙, 等. 口腔微生物组在动脉粥样硬化性心血管疾病中的研究进展[J]. 临床心血管病杂志, 2024, 40(6): 453-456. doi: 10.13201/j.issn.1001-1439.2024.06.006
KAN Jiuxu, YAN Wei, GAO Yunlong, et al. Research progress of oral micro-biome in atherosclerotic cardiovascular disease[J]. J Clin Cardiol, 2024, 40(6): 453-456. doi: 10.13201/j.issn.1001-1439.2024.06.006
Citation: KAN Jiuxu, YAN Wei, GAO Yunlong, et al. Research progress of oral micro-biome in atherosclerotic cardiovascular disease[J]. J Clin Cardiol, 2024, 40(6): 453-456. doi: 10.13201/j.issn.1001-1439.2024.06.006

口腔微生物组在动脉粥样硬化性心血管疾病中的研究进展

  • 基金项目:
    国家自然科学基金(82070336)
详细信息

Research progress of oral micro-biome in atherosclerotic cardiovascular disease

More Information
  • 动脉粥样硬化性心血管疾病(atherosclerotic cardiovascular disease,ASCVD)是引起心血管患者死亡的首要原因,在我国呈逐年上升趋势。已有证据表明,口腔微生物失调所致的牙周疾病可通过全身系统性炎症反应促进ASCVD的发展,但其发生机制及潜在关系目前尚不清楚。因此,本文就口腔微生物和ASCVD的关系,以及口腔微生物失调导致ASCVD的病理生理机制进行阐述,并讨论该领域目前面临的挑战和未来发展方向。
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  • [1]

    Keeter WC, Ma S, Stahr N, et al. Atherosclerosis and multi-organ-associated pathologies[J]. Semin Immunopathol, 2022, 44(3): 363-374. doi: 10.1007/s00281-022-00914-y

    [2]

    《中国心血管健康与疾病报告2021》编写组. 《中国心血管健康与疾病报告2021》要点解读[J]. 中国心血管杂志, 2022, 27(4): 305-318. https://www.cnki.com.cn/Article/CJFDTOTAL-XIXG202304001.htm

    [3]

    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

    [4]

    Xue H, Chen X, Yu C, et al. Gut microbially produced indole-3-propionic acid inhibits atherosclerosis by promoting reverse cholesterol transport and its deficiency is causally related to atherosclerotic cardiovascular disease[J]. Circ Res, 2022, 131(5): 404-420. doi: 10.1161/CIRCRESAHA.122.321253

    [5]

    Sanz M, Marco Del Castillo A, Jepsen S, et al. Periodontitis and cardiovascular diseases: Consensus report[J]. J Clin Periodontol, 2020, 47(3): 268-288. doi: 10.1111/jcpe.13189

    [6]

    Beukers NG, van der Heijden GJ, van Wijk AJ, et al. Periodontitis is an independent risk indicator for atherosclerotic cardiovascular diseases among 60 174 participants in a large dental school in the Netherlands[J]. J Epidemiol Commun Health, 2017, 71(1): 37-42. doi: 10.1136/jech-2015-206745

    [7]

    Park SY, Kim SH, Kang SH, et al. Improved oral hygiene care attenuates the cardiovascular risk of oral health disease: a population-based study from Korea[J]. Eur Heart J, 2019, 40(14): 1138-1145. doi: 10.1093/eurheartj/ehy836

    [8]

    Dotre SV, Davane MS, Nagoba BS. Peridontitis, bacteremia and infective endocarditis: a review study[J]. Arch Pediatr Infect Dis, 2017, 5: e41067.

    [9]

    Cai Z, Lin S, Hu S, et al. Structure and function of oral microbial community in periodontitis based on integrated data[J]. Front Cell Infect Microbiol, 2021, 11: 663756. doi: 10.3389/fcimb.2021.663756

    [10]

    Chhibber-Goel J, Singhal V, Bhowmik D, et al. Linkages between oral commensal bacteria and atherosclerotic plaques in coronary artery disease patients[J]. NPJ Biofilms Microbiomes, 2016, 2: 7. doi: 10.1038/s41522-016-0009-7

    [11]

    Hernández-Ruiz P, Amezcua-Guerra LM, López-Vidal Y, et al. Comparative characterization of inflammatory profile and oral microbiome according to an inflammation-based risk score in ST-segment elevation myocardial infarction[J]. Front Cell Infect Microbiol, 2023, 13: 1095380. doi: 10.3389/fcimb.2023.1095380

    [12]

    Xu AA, Hoffman K, Gurwara S, et al. Oral health and the altered colonic mucosa-associated gut microbiota[J]. Dig Dis Sci, 2021, 66(9): 2981-2991. doi: 10.1007/s10620-020-06612-9

    [13]

    Hashizume-Takizawa T, Yamaguchi Y, Kobayashi R, et al. Oral challenge with Streptococcus sanguinis induces aortic inflammation and accelerates atherosclerosis in spontaneously hyperlipidemic mice[J]. Biochem Biophys Res Commun, 2019, 520(3): 507-513. doi: 10.1016/j.bbrc.2019.10.057

    [14]

    Armingohar Z, Jorgensen JJ, Kristoffersen AK, et al. Bacteria and bacterial DNA in atherosclerotic plaque and aneurysmal wall biopsies from patients with and without periodontitis[J]. J Oral Microbiol, 2014, 6: 110.

    [15]

    Kwun JS, Kang SH, Lee HJ, et al. Comparison of thrombus, gut, and oral microbiomes in Korean patients with ST-elevation myocardial infarction: a case-control study[J]. Exp Mol Med, 2020, 52(12): 2069-2079. doi: 10.1038/s12276-020-00543-1

    [16]

    Kataoka Y, Funabashi S, Doi T, et al. How can we identify very high-risk heterozygous familial hypercholesterolemia?[J]. J Atheroscler Thromb, 2022, 29(6): 795-807. doi: 10.5551/jat.RV17063

    [17]

    Kato-Kogoe N, Sakaguchi S, Kamiya K, et al. Characterization of salivary microbiota in patients with atherosclerotic cardiovascular disease: a case-control study[J]. J Atheroscler Thromb, 2022, 29(3): 403-421. doi: 10.5551/jat.60608

    [18]

    Radaic A, Kapila YL. The oralome and its dysbiosis: New insights into oral microbiome-host interactions[J]. Comput Struct Biotechnol J, 2021, 19: 1335-1360. doi: 10.1016/j.csbj.2021.02.010

    [19]

    Haraszthy Ⅵ, Zambon JJ, Trevisan M, et al. Identification of periodontal pathogens in atheromatous plaques[J]. J Periodontol, 2000, 71(10): 1554-1560. doi: 10.1902/jop.2000.71.10.1554

    [20]

    Fischer RG, Lira JR, Retamal-Valdes B, et al. Periodontal disease and its impact on general health in Latin America. Section Ⅴ: Treatment of periodontitis[J]. Braz Oral Res, 2020, 34: e026. doi: 10.1590/1807-3107bor-2020.vol34.0026

    [21]

    Xu T, Dong Q, Luo Y, et al. Porphyromonas gingivalis infection promotes mitochondrial dysfunction through Drp1-dependent mitochondrial fission in endothelial cells[J]. Int J Oral Sci, 2021, 13(1): 28. doi: 10.1038/s41368-021-00134-4

    [22]

    Schenkein HA, Papapanou PN, Genco R, et al. Mechanisms underlying the association between periodontitis and atherosclerotic disease[J]. Periodontol, 2020, 83(1): 90-106. doi: 10.1111/prd.12304

    [23]

    Fernandes D, Khambata RS, Massimo G, et al. Local delivery of nitric oxide prevents endothelial dysfunction in periodontitis[J]. Pharmacol Res, 2023, 188: 106616. doi: 10.1016/j.phrs.2022.106616

    [24]

    Yee M, Kim S, Sethi P, et al. Porphyromonasgingivalis stimulates IL-6 and IL-8 secretion in GMSM-K, HSC-3 and H413 oral epithelial cells[J]. Anaerobe, 2014, 28, 62-67.

    [25]

    Tonelli A, Lumngwena EN, Ntusi N. The oral microbiome in the pathophysiology of cardiovascular disease[J]. Nat Rev Cardiol, 2023, 20(6): 386-403. doi: 10.1038/s41569-022-00825-3

    [26]

    Zhong M, Huang J, Wu Z, et al. Potential roles of selectins in periodontal diseases and associated systemic diseases: could they be targets for immunotherapy?[J]. Int J Mol Sci, 2022, 23(22): 110.

    [27]

    Lam FW, Brown CA, Valladolid C, et al. The vimentin rod domain blocks P-selectin-P-selectin glycoprotein ligand 1 interactions to attenuate leukocyte adhesion to inflamed endothelium[J]. PLoS One, 2020, 15(10): e0240164. doi: 10.1371/journal.pone.0240164

    [28]

    Liljestrand JM, Paju S, Pietiäinen M, et al. Immunologic burden links periodontitis to acute coronary syndrome[J]. Atherosclerosis, 2018, 268: 177-184. doi: 10.1016/j.atherosclerosis.2017.12.007

    [29]

    Tong Y, Xin Y, Fu L, et al. Excessive neutrophil extracellular trap formation induced by Porphyromonas gingivalis lipopolysaccharide exacerbates inflammatory responses in high glucose microenvironment[J]. Front Cell Infect Microbiol, 2023, 13: 1108228. doi: 10.3389/fcimb.2023.1108228

    [30]

    Lönn J, Ljunggren S, Klarström-Engström K, et al. Lipoprotein modifications by gingipains of Porphyromonas gingivalis[J]. J Periodontal Res, 2018, 53(3): 403-413. doi: 10.1111/jre.12527

    [31]

    Aarabi G, Heydecke G, Seedorf U. Roles of oral infections in the pathomechanism of atherosclerosis[J]. Int J Mol Sci, 2018, 19(7): 110.

    [32]

    Hansen PR, Holmstrup P. Cardiovascular diseases and periodontitis[J]. Adv Exp Med Biol, 2022, 1373, 261-280.

    [33]

    Gurav AN. The implication of periodontitis in vascular endothelial dysfunction[J]. Eur J Clin Invest, 2014, 44(10): 1000-1009.

    [34]

    Suárez LJ, Garzón H, Arboleda S, et al. Oral dysbiosis and autoimmunity: from local periodontal responses to an imbalanced systemic immunity. a review[J]. Front Immunol, 2020, 11: 591255.

    [35]

    Wick G, Jakic B, Buszko M, et al. The role of heat shock proteins in atherosclerosis[J]. Nat Rev Cardiol, 2014, 11(9): 516-529.

    [36]

    任阳荷, 王红, 李为民. PCSK9通过非低密度脂蛋白胆固醇途径影响心血管疾病的研究进展[J]. 临床心血管病杂志, 2023, 39(7): 563-567. https://lcxxg.whuhzzs.com/article/doi/10.13201/j.issn.1001-1439.2023.07.014

    [37]

    Rosenson RS, Brewer HB Jr, Barter PJ, et al. HDL and atherosclerotic cardiovascular disease: genetic insights into complex biology[J]. Nat Rev Cardiol, 2018, 15(1): 9-19.

    [38]

    Tong Y, Xin Y, Fu L, et al. Excessive neutrophil extracellular trap formation induced by Porphyromonas gingivalis lipopolysaccharide exacerbates inflammatory responses in high glucose microenvironment[J]. Front Cell Infect Microbiol, 2023, 13: 1108228.

    [39]

    Borén J, Chapman MJ, Krauss RM, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel[J]. Eur Heart J, 2020, 41(24): 2313-2330. http://www.bmj.com/lookup/external-ref?access_num=32052833&link_type=MED&atom=%2Fbmj%2F368%2Fbmj.m744.atom

    [40]

    Kim HJ, Cha GS, Kim HJ, et al. Porphyromonas gingivalis accelerates atherosclerosis through oxidation of high-density lipoprotein[J]. J Periodontal Implant Sci, 2018, 48(1): 60-68.

    [41]

    Lönn J, Ljunggren S, Klarström-Engström K, et al. Lipoprotein modifications by gingipains of Porphyromonas gingivalis[J]. J Periodontal Res, 2018, 53(3): 403-413.

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出版历程
收稿日期:  2023-07-18
刊出日期:  2024-06-13

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