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Review
. 2023 Feb 23;12(5):707.
doi: 10.3390/cells12050707.

Hypotheses on Atherogenesis Triggering: Does the Infectious Nature of Atherosclerosis Development Have a Substruction?

Affiliations
Review

Hypotheses on Atherogenesis Triggering: Does the Infectious Nature of Atherosclerosis Development Have a Substruction?

Konstantin A Lusta et al. Cells. .

Abstract

Since the end of the 20th century, it has been clear that atherosclerosis is an inflammatory disease. However, the main triggering mechanism of the inflammatory process in the vascular walls is still unclear. To date, many different hypotheses have been put forward to explain the causes of atherogenesis, and all of them are supported by strong evidence. Among the main causes of atherosclerosis, which underlies these hypotheses, the following can be mentioned: lipoprotein modification, oxidative transformation, shear stress, endothelial dysfunction, free radicals' action, homocysteinemia, diabetes mellitus, and decreased nitric oxide level. One of the latest hypotheses concerns the infectious nature of atherogenesis. The currently available data indicate that pathogen-associated molecular patterns from bacteria or viruses may be an etiological factor in atherosclerosis. This paper is devoted to the analysis of existing hypotheses for atherogenesis triggering, and special attention is paid to the contribution of bacterial and viral infections to the pathogenesis of atherosclerosis and cardiovascular disease.

Keywords: atherosclerosis; cardiovascular disease; cytokines; endothelial dysfunction; infections; inflammation; lipoprotein modification; pathogen-associated molecular patterns.

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Conflict of interest statement

The authors declare no conflict of interest.

References

    1. Chistiakov D.A., Myasoedova V.A., Melnichenko A.A., Grechko A.V., Orekhov A.N. Calcifying Matrix Vesicles and Atherosclerosis. Biomed. Res. Int. 2017;2017:7463590. doi: 10.1155/2017/7463590. - DOI - PMC - PubMed
    1. WHO CVD Risk Chart Working Group World Health Organization cardiovascular disease risk charts: Revised models to estimate risk in 21 global regions. Lancet Glob. Health. 2019;7:e1332–e1345. doi: 10.1016/S2214-109X(19)30318-3. - DOI - PMC - PubMed
    1. Brophy M.L., Dong Y., Wu H., Rahman H.N., Song K., Chen H. Eating the Dead to Keep Atherosclerosis at Bay. Front. Cardiovasc. Med. 2017;4:2. doi: 10.3389/fcvm.2017.00002. - DOI - PMC - PubMed
    1. Ross R. Atherosclerosis is an inflammatory disease. Am. Heart J. 1999;138:S419–S420. doi: 10.1016/S0002-8703(99)70266-8. - DOI - PubMed
    1. Pothineni N.V.K., Subramany S., Kuriakose K., Shirazi L.F., Romeo F., Shah P.K., Mehta J.L. Infections, atherosclerosis, and coronary heart disease. Eur. Heart J. 2017;38:3195–3201. doi: 10.1093/eurheartj/ehx362. - DOI - PubMed

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