TY - JOUR

T1 - Atherosclerosis, Cardiovascular Disorders and COVID-19: Comorbid Pathogenesis

AU - Makarova , Yulia A.

AU - Ryabkova, Varvara A.

AU - Salukhov, Vladimir V.

AU - Sagun, Boris V.

AU - Korovin , Aleksandr E.

AU - Churilov, Leonid P.

N1 - Makarova, Y.A.; Ryabkova, V.A.; Salukhov, V.V.; Sagun, B.V.; Korovin, A.E.; Churilov, L.P. Atherosclerosis, Cardiovascular Disorders and COVID-19: Comorbid Pathogenesis. Diagnostics 2023, 13, 478. https://doi.org/10.3390/diagnostics13030478

PY - 2023/1/28

Y1 - 2023/1/28

N2 - The article describes how atherosclerosis and coronavirus disease 19 (COVID-19) mayaffect each other. The features of this comorbid pathogenesis at various levels (vascular, cellular and molecular) are considered. A bidirectional influence of these conditions is described: the presence of cardiovascular diseases affects different individuals’ susceptibility to viral infection. In turn, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can have a negative effect on the endothelium and cardiomyocytes, causing blood clotting, secretion of pro-inflammatory cytokines, and thus exacerbating the development of atherosclerosis. In addition to the established entry into cells via angiotensin-converting enzyme 2 (ACE2), other mechanisms of SARS-CoV-2 entry are currently under investigation, for example, through CD147. Pathogenesis of comorbidity can be determined by the influence of the virus on various links which are meaningful for atherogenesis:generation of oxidized forms of low-density lipoproteins (LDL), launch of a cytokine storm, damage to the endothelial glycocalyx, and mitochondrial injury. The transformation of a stable plaque into an unstable one plays an important role in the pathogenesis of atherosclerosis complications and can be triggered by COVID-19. The impact of SARS-CoV-2 on large vessels such as the aorta is more complex than previously thought considering its impact on vasa vasorum. Current information on the mutual influence of the medicines used in the treatment of atherosclerosis and acute COVID-19 is briefly summarized.

AB - The article describes how atherosclerosis and coronavirus disease 19 (COVID-19) mayaffect each other. The features of this comorbid pathogenesis at various levels (vascular, cellular and molecular) are considered. A bidirectional influence of these conditions is described: the presence of cardiovascular diseases affects different individuals’ susceptibility to viral infection. In turn, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can have a negative effect on the endothelium and cardiomyocytes, causing blood clotting, secretion of pro-inflammatory cytokines, and thus exacerbating the development of atherosclerosis. In addition to the established entry into cells via angiotensin-converting enzyme 2 (ACE2), other mechanisms of SARS-CoV-2 entry are currently under investigation, for example, through CD147. Pathogenesis of comorbidity can be determined by the influence of the virus on various links which are meaningful for atherogenesis:generation of oxidized forms of low-density lipoproteins (LDL), launch of a cytokine storm, damage to the endothelial glycocalyx, and mitochondrial injury. The transformation of a stable plaque into an unstable one plays an important role in the pathogenesis of atherosclerosis complications and can be triggered by COVID-19. The impact of SARS-CoV-2 on large vessels such as the aorta is more complex than previously thought considering its impact on vasa vasorum. Current information on the mutual influence of the medicines used in the treatment of atherosclerosis and acute COVID-19 is briefly summarized.

KW - atherosclerosis

KW - COVID-19

KW - inflammation

KW - cardiovascular system

KW - cytokines

KW - endothelium

KW - lipoproteins

KW - renin-angiotensin system

KW - ATHEROMA

KW - autoimmunity

KW - vasa vasorum

KW - atheroma

UR - https://www.mendeley.com/catalogue/44e7a58c-f6b3-3ebc-a33e-822a18bd7ff7/

U2 - https://doi.org/10.3390/diagnostics13030478

DO - https://doi.org/10.3390/diagnostics13030478

M3 - Review article

C2 - 36766583

VL - 13

JO - Diagnostics

JF - Diagnostics

SN - 2075-4418

IS - 3

M1 - 478

ER -