2022
DOI: 10.1016/j.lfs.2022.121018
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Long-term effect of SARS-CoV-2 infection on cardiovascular outcomes and all-cause mortality

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Cited by 25 publications
(23 citation statements)
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“…Damaged mitochondria are sources of products of incomplete oxygen reduction, i.e., ROS, which play an important role in the pathogenesis of atherogenesis [33] SARS-CoV-2 infection may also promote telomere shortening by exporting the TERF2IP-TRF2 complex following mitochondrial ROS (mtROS) -mediated activation of the ribosomal s6-kinase p90RSK. Thus, it is possible that oxidative stress caused by SARS-CoV-2 infection may contribute to aging phenotypes that exacerbate the development and progression of atherosclerosis in COVID-19 survivors [20]. This is consistent with the theory of atherogenesis as a manifestation of local clonal aging and deterioration of the vascular cells [7].…”
Section: Respiratory Failure and Mixed Hypoxiasupporting
confidence: 78%
See 1 more Smart Citation
“…Damaged mitochondria are sources of products of incomplete oxygen reduction, i.e., ROS, which play an important role in the pathogenesis of atherogenesis [33] SARS-CoV-2 infection may also promote telomere shortening by exporting the TERF2IP-TRF2 complex following mitochondrial ROS (mtROS) -mediated activation of the ribosomal s6-kinase p90RSK. Thus, it is possible that oxidative stress caused by SARS-CoV-2 infection may contribute to aging phenotypes that exacerbate the development and progression of atherosclerosis in COVID-19 survivors [20]. This is consistent with the theory of atherogenesis as a manifestation of local clonal aging and deterioration of the vascular cells [7].…”
Section: Respiratory Failure and Mixed Hypoxiasupporting
confidence: 78%
“…In vitro infection of cardiomyocytes with the S1 subunits of the SARS-CoV-2 spike protein can alter their transcriptome, induce fragmentation of myofibrils, and destruction of nuclei. Thus, the S1 protein itself is dangerous for cardiac cells, and SARS-CoV-2 is characterized by the ability to cause hypertrophic myocardial remodeling, cardiac dysfunction, and myocarditis [20]. In coronavirus myocarditis (as in myocarditis caused by enteroviruses and herpes group viruses), both lymphocytic infiltration of the myocardium and autoantibodies against cardiac antigens are detected [21].…”
Section: Direct and Immune-related Cytopathic Effects Of Sars-cov-2 O...mentioning
confidence: 99%
“…315 Whether SARS-CoV-2 interacts with the gut microbiota to modulate COVID-19–related CVD risk remains unknown. 316,317…”
Section: Interaction Between the Gut Microbiome And Viral Infection I...mentioning
confidence: 99%
“…Potential mechanisms related to the pathophysiology of long COVID-19 could include (1) harm to tissues and cells that are relevant for vascular flow, therefore blood clotting is increased; (2) persistence of fragments of the virus or its sub-particles/protein material in a wide range of tissues; and (3) an altered immune system, among others. Moreover, chronic cardiovascular effects of COVID-19 have been frequently reported, even among those who had no previous CVD, suggesting an important tropism of this virus with the cardiovascular system [ 5 ]. Therefore, heart disease patients are specifically considered to have a worse prognosis during the acute phase of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection [ 6 , 7 , 8 , 9 , 10 ].…”
Section: Introductionmentioning
confidence: 99%