Erschienen in:
31.07.2022 | COVID-19 | Comment
Type 2 alveolar epithelial cell-derived circulating extracellular vesicle-encapsulated surfactant protein C as a mediator of cardiac inflammation in COVID-19
verfasst von:
Mohammad Rudiansyah, Ermias Mergia Terefe, Maria Jade Catalan Opulencia, Walid Kamal Abdelbasset, Dmitry Olegovich Bokov, Amr A. El-Sehrawy, Sayfiddin Baymakov, Ali Thaeer Hammid, Milad Shirvaliloo, Reza Akhavan‐Sigari
Erschienen in:
Inflammation Research
|
Ausgabe 9/2022
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Abstract
Among the countless endeavours made at elucidating the pathogenesis of COVID-19, those aimed at the histopathological alterations of type 2 alveolar epithelial cells (AT2) are of outstanding relevance to the field of lung physiology, as they are the building blocks of the pulmonary alveoli. A merit of high regenerative and proliferative capacity, exocytotic activity resulting in the release of extracellular vesicles (EVs) is particularly high in AT2 cells, especially in those infected with SARS-CoV-2. These AT2 cell-derived EVs, containing the genetic material of the virus, might enter the bloodstream and make their way into the cardiovascular system, where they may infect cardiomyocytes and bring about a series of events leading to heart failure. As surfactant protein C, a marker of AT2 cell activity and a constituent of the lung surfactant complex, occurs abundantly inside the AT2-derived EVs released during the inflammatory stage of COVID-19, it could potentially be used as a biomarker for predicting impending heart failure in those patients with a history of cardiovascular disease.