ENDOTHELIAL DYSFUNCTION AND PULMONARY LESIONS IN LONG-COVID
DOI:
https://doi.org/10.11603/1681-2727.2025.2.15300Keywords:
Long-COVID, COVID-19, endothelial dysfunction, biological markers, respiratory system, strong healthAbstract
This review analyzed current scientific research data regarding the role of endothelial dysfunction in the pathogenesis of Long-COVID, specifically examining its impact on the alveolar-capillary membrane and the development of pulmonary complications. The potential of endothelial dysfunction biomarkers for diagnosis, prognosis, and the development of new therapeutic strategies was evaluated.
Analysis of open scientific data revealed that SARS-CoV-2-induced endothelial dysfunction was a key factor in the development of Long-COVID, leading to alterations in the alveolar-capillary membrane. Consequently, the development of interstitial lung diseases with fibrosis, impaired diffusion, and microcirculation was initiated, resulting in decreased tissue oxygenation. The pivotal role of endothelial function and alveolar epithelial status disorders, reflected in changes in Angiopoietin-1 (Ang-1), Angiopoietin-2 (Ang-2), von Willebrand factor (vWF), P-selectin, Intercellular adhesion molecule 1 (ICAM-1), Vascular endothelial growth factor (VEGF), and Krebs von den Lungen-6 (KL-6) levels, in the development and severity of pulmonary complications in patients with post-COVID syndrome was established.
This study expands the scientific and practical knowledge of medical professionals regarding the role of endothelial dysfunction biomarkers in the development of pulmonary complications associated with Long-COVID, and demonstrates their potential for diagnosis, prognosis, and the development of new therapeutic strategies.
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