Vascular Aging and COVID-19
Badaras, Ignas and Laučytė-Cibulskienė, Agnė LU
(2023)
In Angiology
74(4).
p.308-316
- Abstract
Vascular age is determined by functional and structural changes in the arterial wall. When measured by its proxy, pulse wave velocity, it has been shown to predict cardiovascular and total mortality. Disconcordance between chronological and vascular age might represent better or worse vascular health. Cell senescence is caused by oxidative stress and sustained cell replication. Senescent cells acquire senescence-associated secretory phenotype. Oxidative stress, endothelial dysfunction, dysregulation of coagulation and leucocyte infiltration are observed in the aging endothelium. All of these mechanisms lead to increased vascular calcification and stiffness. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can involve the... (More)
Vascular age is determined by functional and structural changes in the arterial wall. When measured by its proxy, pulse wave velocity, it has been shown to predict cardiovascular and total mortality. Disconcordance between chronological and vascular age might represent better or worse vascular health. Cell senescence is caused by oxidative stress and sustained cell replication. Senescent cells acquire senescence-associated secretory phenotype. Oxidative stress, endothelial dysfunction, dysregulation of coagulation and leucocyte infiltration are observed in the aging endothelium. All of these mechanisms lead to increased vascular calcification and stiffness. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can involve the vascular endothelium. It enters cells using angiotensin-converting enzyme 2 (ACE-2) receptors, which are abundant in endothelial cells. The damage this virus does to the endothelium can be direct or indirect. Indirect damage is caused by hyperinflammation. Direct damage results from effects on ACE-2 receptors. The reduction of ACE-2 levels seen during coronavirus disease 2019 (COVID-19) infection might cause vasoconstriction and oxidative stress. COVID-19 and vascular aging share some pathways. Due to the novelty of the virus, there is an urgent need for studies that investigate its long-term effects on vascular health.
(Less)
- author
- Badaras, Ignas
and Laučytė-Cibulskienė, Agnė
LU
- organization
- publishing date
- 2023
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- angiotensin-converting enzyme 2, coronavirus disease 2019, endothelial senescence, pulse wave velocity, vascular aging
- in
- Angiology
- volume
- 74
- issue
- 4
- pages
- 308 - 316
- publisher
- SAGE Publications
- external identifiers
-
- pmid:36031949
- scopus:85138010869
- ISSN
- 0003-3197
- DOI
- 10.1177/00033197221121007
- language
- English
- LU publication?
- yes
- id
- 93ae72db-7194-43c5-8c14-4fd8507b15ef
- date added to LUP
- 2022-12-05 09:16:32
- date last changed
- 2024-04-18 17:35:01
@article{93ae72db-7194-43c5-8c14-4fd8507b15ef,
abstract = {{<p>Vascular age is determined by functional and structural changes in the arterial wall. When measured by its proxy, pulse wave velocity, it has been shown to predict cardiovascular and total mortality. Disconcordance between chronological and vascular age might represent better or worse vascular health. Cell senescence is caused by oxidative stress and sustained cell replication. Senescent cells acquire senescence-associated secretory phenotype. Oxidative stress, endothelial dysfunction, dysregulation of coagulation and leucocyte infiltration are observed in the aging endothelium. All of these mechanisms lead to increased vascular calcification and stiffness. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can involve the vascular endothelium. It enters cells using angiotensin-converting enzyme 2 (ACE-2) receptors, which are abundant in endothelial cells. The damage this virus does to the endothelium can be direct or indirect. Indirect damage is caused by hyperinflammation. Direct damage results from effects on ACE-2 receptors. The reduction of ACE-2 levels seen during coronavirus disease 2019 (COVID-19) infection might cause vasoconstriction and oxidative stress. COVID-19 and vascular aging share some pathways. Due to the novelty of the virus, there is an urgent need for studies that investigate its long-term effects on vascular health.</p>}},
author = {{Badaras, Ignas and Laučytė-Cibulskienė, Agnė}},
issn = {{0003-3197}},
keywords = {{angiotensin-converting enzyme 2; coronavirus disease 2019; endothelial senescence; pulse wave velocity; vascular aging}},
language = {{eng}},
number = {{4}},
pages = {{308--316}},
publisher = {{SAGE Publications}},
series = {{Angiology}},
title = {{Vascular Aging and COVID-19}},
url = {{http://dx.doi.org/10.1177/00033197221121007}},
doi = {{10.1177/00033197221121007}},
volume = {{74}},
year = {{2023}},
}