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Role of oral microbiota in atherosclerosis.

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Title: Role of oral microbiota in atherosclerosis.
Authors: Liu, Xiang-Rui1 (AUTHOR), Xu, Qian1 (AUTHOR), Xiao, Jun1 (AUTHOR), Deng, Yi-Ming1 (AUTHOR), Tang, Zhi-Han1 (AUTHOR), Tang, Ya-Ling1 (AUTHOR) tangyaling7508@163.com, Liu, Lu-Shan1 (AUTHOR) liuls2000@163.com
Source: Clinica Chimica Acta. Jul2020, Vol. 506, p191-195. 5p.
Subjects: Atherosclerosis, Atherosclerotic plaque, Oral diseases, Blood lipids, Heart diseases, Oral mucosa, Macrophages
Abstract: • Atherosclerosis is a chronic inflammatory disease characterized by the development of lipid-rich plaques; • Oral infection induces atherosclerosis through local and systemic inflammatory responses; • Oral infection promotes the formation of macrophage-derived foam cells and affects lipid levels. Oral infections are common among individuals of all ages and can activate local and systemic inflammation. The inflammatory response plays an important role in atherosclerosis. An increasing number of studies have reported an association between oral pathogen infection and atherosclerotic coronary heart disease. For instance, epidemiological studies support the positive correlation between oral infections and atherosclerosis. The presence of oral pathogens in human atherosclerotic plaques has been detected by multiple methods, and oral infections promote atherosclerosis in animal experiments. Various mechanisms are involved in oral infections, thereby promoting atherosclerosis. First, oral infections can trigger the local and systemic inflammatory response, causing vascular endothelial damage. Oral-derived pathogens that enter atherosclerotic plaque can activate macrophages and cause an intra-plaque inflammatory response. Second, oral infections can promote intra-plaque macrophage cholesterol accumulation and foam cell formation. Third, oral infections can regulate plasma lipid levels, thereby increasing atherogenic lipid low-density lipoprotein and triglyceride levels. Although atherosclerosis caused by oral infections is currently studied, the precise mechanism remains to be further explored. The rise of gut microbiota research also makes the relationship between oral microbiota and disease, especially the relationship with coronary heart disease, worthy of attention and in-depth research. [ABSTRACT FROM AUTHOR]
Copyright of Clinica Chimica Acta is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Engineering Source
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Header DbId: egs
DbLabel: Engineering Source
An: 143247510
AccessLevel: 6
PubType: Academic Journal
PubTypeId: academicJournal
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  Data: Role of oral microbiota in atherosclerosis.
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  Data: <searchLink fieldCode="AR" term="%22Liu%2C+Xiang-Rui%22">Liu, Xiang-Rui</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Xu%2C+Qian%22">Xu, Qian</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Xiao%2C+Jun%22">Xiao, Jun</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Deng%2C+Yi-Ming%22">Deng, Yi-Ming</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Tang%2C+Zhi-Han%22">Tang, Zhi-Han</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Tang%2C+Ya-Ling%22">Tang, Ya-Ling</searchLink><relatesTo>1</relatesTo> (AUTHOR)<i> tangyaling7508@163.com</i><br /><searchLink fieldCode="AR" term="%22Liu%2C+Lu-Shan%22">Liu, Lu-Shan</searchLink><relatesTo>1</relatesTo> (AUTHOR)<i> liuls2000@163.com</i>
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  Data: <searchLink fieldCode="JN" term="%22Clinica+Chimica+Acta%22">Clinica Chimica Acta</searchLink>. Jul2020, Vol. 506, p191-195. 5p.
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  Data: <searchLink fieldCode="DE" term="%22Atherosclerosis%22">Atherosclerosis</searchLink><br /><searchLink fieldCode="DE" term="%22Atherosclerotic+plaque%22">Atherosclerotic plaque</searchLink><br /><searchLink fieldCode="DE" term="%22Oral+diseases%22">Oral diseases</searchLink><br /><searchLink fieldCode="DE" term="%22Blood+lipids%22">Blood lipids</searchLink><br /><searchLink fieldCode="DE" term="%22Heart+diseases%22">Heart diseases</searchLink><br /><searchLink fieldCode="DE" term="%22Oral+mucosa%22">Oral mucosa</searchLink><br /><searchLink fieldCode="DE" term="%22Macrophages%22">Macrophages</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: • Atherosclerosis is a chronic inflammatory disease characterized by the development of lipid-rich plaques; • Oral infection induces atherosclerosis through local and systemic inflammatory responses; • Oral infection promotes the formation of macrophage-derived foam cells and affects lipid levels. Oral infections are common among individuals of all ages and can activate local and systemic inflammation. The inflammatory response plays an important role in atherosclerosis. An increasing number of studies have reported an association between oral pathogen infection and atherosclerotic coronary heart disease. For instance, epidemiological studies support the positive correlation between oral infections and atherosclerosis. The presence of oral pathogens in human atherosclerotic plaques has been detected by multiple methods, and oral infections promote atherosclerosis in animal experiments. Various mechanisms are involved in oral infections, thereby promoting atherosclerosis. First, oral infections can trigger the local and systemic inflammatory response, causing vascular endothelial damage. Oral-derived pathogens that enter atherosclerotic plaque can activate macrophages and cause an intra-plaque inflammatory response. Second, oral infections can promote intra-plaque macrophage cholesterol accumulation and foam cell formation. Third, oral infections can regulate plasma lipid levels, thereby increasing atherogenic lipid low-density lipoprotein and triglyceride levels. Although atherosclerosis caused by oral infections is currently studied, the precise mechanism remains to be further explored. The rise of gut microbiota research also makes the relationship between oral microbiota and disease, especially the relationship with coronary heart disease, worthy of attention and in-depth research. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of Clinica Chimica Acta is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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RecordInfo BibRecord:
  BibEntity:
    Identifiers:
      – Type: doi
        Value: 10.1016/j.cca.2020.03.033
    Languages:
      – Code: eng
        Text: English
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      Pagination:
        PageCount: 5
        StartPage: 191
    Subjects:
      – SubjectFull: Atherosclerosis
        Type: general
      – SubjectFull: Atherosclerotic plaque
        Type: general
      – SubjectFull: Oral diseases
        Type: general
      – SubjectFull: Blood lipids
        Type: general
      – SubjectFull: Heart diseases
        Type: general
      – SubjectFull: Oral mucosa
        Type: general
      – SubjectFull: Macrophages
        Type: general
    Titles:
      – TitleFull: Role of oral microbiota in atherosclerosis.
        Type: main
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          Name:
            NameFull: Liu, Xiang-Rui
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            NameFull: Xu, Qian
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            NameFull: Xiao, Jun
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            NameFull: Deng, Yi-Ming
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            NameFull: Tang, Zhi-Han
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              M: 07
              Text: Jul2020
              Type: published
              Y: 2020
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              Value: 506
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            – TitleFull: Clinica Chimica Acta
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