Endothelial Dysfunction as a Primary Consequence of SARS-CoV-2 Infection

Mezoh, Genevieve; Crowther, Nigel J

doi:10.1007/978-3-030-59261-5_3

Cited by 13 publications

(12 citation statements)

References 68 publications

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“…Endothelial cells are rich in ACE2, hence, the virus itself can directly cause dysfunction by simply infecting the cells [ 42 ]. Additionally, when SARS-CoV-2 infect cells neighboring endothelial cells, an increase in inflammation and cytokine factors can be observed which will, after prolonged exposure, stimulate endothelial dysfunction [ 43 ].…”

Section: Early Ageing Alterations In Endothelial and Adipose Tissue Of Covid-19 Patientsmentioning

confidence: 99%

“…Endothelial dysfunction plays a pivotal role in the development of COVID-19. It will lead to apoptosis and the loosening of cell-cell interactions between the endothelial cells [ 43 ], which will increase the vascular permeability. This will reduce the barrier function and allow the vascular leakage and transportation of the virus to other organs with a high expression of ACE2 resulting in COVID-19 patients with dysfunction of multiple organs.…”

Section: Early Ageing Alterations In Endothelial and Adipose Tissue Of Covid-19 Patientsmentioning

confidence: 99%

“…Moreover, endothelial dysfunction will activate the coagulation cascade, which induces thrombus formation. Finally, it will increase inflammation and lead to cytokine storm, which will aggravate the disease [ 43 , 44 , 45 ].…”

Section: Early Ageing Alterations In Endothelial and Adipose Tissue Of Covid-19 Patientsmentioning

confidence: 99%

“…Moreover, SARS-CoV-2 also stimulates a variety of T-cells to promote the production of IL-1β and IL-6, and recruit more immune cells to produce cytokines, which can further contribute to the development of the cytokine dysregulation [ 78 ]. The systemic inflammation and the overstimulation of the immune response will contribute to endothelial and adipose tissue dysfunction, and neuronal sensitization [ 43 , 58 , 63 ]. This can be the trigger for OA-like changes in COVID-19 patients.…”

Section: Exploring Underlying Molecular Mechanismsmentioning

confidence: 99%

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COVID-19 in Joint Ageing and Osteoarthritis: Current Status and Perspectives

Lauwers

Yuan

et al. 2022

IJMS

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COVID-19 is a trending topic worldwide due to its immense impact on society. Recent trends have shifted from acute effects towards the long-term morbidity of COVID-19. In this review, we hypothesize that SARS-CoV-2 contributes to age-related perturbations in endothelial and adipose tissue, which are known to characterize the early aging process. This would explain the long-lasting symptoms of SARS-CoV-2 as the result of an accelerated aging process. Connective tissues such as adipose tissue and musculoskeletal tissue are the primary sites of aging. Therefore, current literature was analyzed focusing on the musculoskeletal symptoms in COVID-19 patients. Hypovitaminosis D, increased fragility, and calcium deficiency point towards bone aging, while joint and muscle pain are typical for joint and muscle aging, respectively. These characteristics could be classified as early osteoarthritis-like phenotype. Exploration of the impact of SARS-CoV-2 and osteoarthritis on endothelial and adipose tissue, as well as neuronal function, showed similar perturbations. At a molecular level, this could be attributed to the angiotensin-converting enzyme 2 expression, renin-angiotensin system dysfunction, and inflammation. Finally, the influence of the nicotinic cholinergic system is being evaluated as a new treatment strategy. This is combined with the current knowledge of musculoskeletal aging to pave the road towards the treatment of long-term COVID-19.

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Section: Early Ageing Alterations In Endothelial and Adipose Tissue Of Covid-19 Patientsmentioning

confidence: 99%

Section: Early Ageing Alterations In Endothelial and Adipose Tissue Of Covid-19 Patientsmentioning

confidence: 99%

Section: Early Ageing Alterations In Endothelial and Adipose Tissue Of Covid-19 Patientsmentioning

confidence: 99%

Section: Exploring Underlying Molecular Mechanismsmentioning

confidence: 99%

See 2 more Smart Citations

COVID-19 in Joint Ageing and Osteoarthritis: Current Status and Perspectives

Lauwers

Yuan

et al. 2022

IJMS

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“…These reduced presentations occurred despite an increased risk for both acute thrombotic events [ 1 – 4 ] and intracranial hemorrhages [ 5 – 7 ] in patients with COVID-19. The SARS-CoV-2 virus can infect the vascular endothelial cells, which abundantly express ACE-2 (angiotensin-converting enzyme-2) [ 8 – 10 ], the entry receptor of the virus. There is increasing evidence causally linking SARS-CoV-2 infection to both microvascular and macrovascular pathologies, resulting in a wide range of neurological consequences, from development of multiple cerebral microhemorrhages and lacunar infarcts [ 11 – 14 ] to larger ischemic strokes [ 3 , 4 ] and intracerebral hemorrhages [ 5 – 7 ].…”

Section: Introductionmentioning

confidence: 99%

Stringent public health measures during COVID-19 across ischemic stroke care systems: the potential impact of patient perceptions on health care-seeking behaviors

et al. 2022

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Decreases in acute stroke presentations have been reported during the coronavirus disease 2019 (COVID-19) pandemic surges. A recent study by Bojti et al. ( GeroScience . 2021;43:2231–2248) sought to understand the relationship of public health mandates in Hungary as they were implemented with acute ischemic stroke admissions and interventions during two separate COVID-19 waves. We sought to perform a similar analysis of changes in ischemic stroke care at two distinct medical institutions in the USA. Two separate institutions and systems of ischemic stroke care were evaluated through a regional comprehensive stroke center telestroke service and a Veterans Affairs (VA) inpatient stroke and neurorehabilitation service. Telestroke consultations in a single system in Chicago, IL, were significantly decreased during the first COVID-19 wave during severely restricted public health mandates ( z -score < − 2), and were less depressed during a subsequent wave with less severe restrictions ( z -score approaching − 1), which resembles findings in Hungary as reported by Bojti et al. In contrast, inpatient admissions during the first and second COVID-19 waves to a VA stroke and neurorehabilitation service in Oklahoma City remained unchanged. The Chicago and Hungary patterns of stroke presentations suggest that public perceptions, as informed by regional health mandates, might influence healthcare-seeking behavior. However, the VA experience suggests that specific patient populations may react differently to given public health mandates. These observations highlight that changes in stroke presentation during the COVID-19 pandemic may vary regionally and by patient population as well as by the severity of public health mandates implemented. Further study of COVID-19-related public health policies on acute stroke populations is needed to capture the long-term impact of such policies. Learning from the real-time impact of pandemic surges and public health policy on presentation of acute medical conditions, such as ischemic stroke, may prove valuable for designing effective policies in the future.

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