Endothelial Dysfunction in COVID-19: Potential Mechanisms and Possible Therapeutic Options
SARS-CoV-2, a novel coronavirus found in Wuhan (China) at the end of 2019, is the etiological agent of the current pandemic that is a heterogeneous disease, named coronavirus disease 2019 (COVID-19). SARS-CoV-2 affects primarily the lungs, but it can induce multi-organ involvement such as acute myoc...
| Main Authors: | , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2022-10-01
|
| Series: | Life |
| Subjects: | |
| Online Access: | https://www.mdpi.com/2075-1729/12/10/1605 |
| _version_ | 1797472013557694464 |
|---|---|
| author | Maria Chiara Pelle Isabella Zaffina Stefania Lucà Valentina Forte Vincenzo Trapanese Melania Melina Federica Giofrè Franco Arturi |
| author_facet | Maria Chiara Pelle Isabella Zaffina Stefania Lucà Valentina Forte Vincenzo Trapanese Melania Melina Federica Giofrè Franco Arturi |
| author_sort | Maria Chiara Pelle |
| collection | DOAJ |
| description | SARS-CoV-2, a novel coronavirus found in Wuhan (China) at the end of 2019, is the etiological agent of the current pandemic that is a heterogeneous disease, named coronavirus disease 2019 (COVID-19). SARS-CoV-2 affects primarily the lungs, but it can induce multi-organ involvement such as acute myocardial injury, myocarditis, thromboembolic eventsandrenal failure. Hypertension, chronic kidney disease, diabetes mellitus and obesity increase the risk of severe complications of COVID-19. There is no certain explanation for this systemic COVID-19 involvement, but it could be related to endothelial dysfunction, due to direct (endothelial cells are infected by the virus) and indirect damage (systemic inflammation) factors. Angiotensin-converting enzyme 2 (ACE2), expressed in human endothelium, has a fundamental role in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. In fact, ACE2 is used as a receptor by SARS-CoV-2, leading to the downregulation of these receptors on endothelial cells; once inside, this virus reduces the integrity of endothelial tissue, with exposure of prothrombotic molecules, platelet adhesion, activation of coagulation cascades and, consequently, vascular damage. Systemic microangiopathy and thromboembolism can lead to multi-organ failure with an elevated risk of death. Considering the crucial role of the immunological response and endothelial damage in developing the severe form of COVID-19, in this review, we will attempt to clarify the underlying pathophysiological mechanisms. |
| first_indexed | 2024-03-09T19:56:05Z |
| format | Article |
| id | doaj.art-915e5f4d988847a2a84aba4fa42260de |
| institution | Directory Open Access Journal |
| issn | 2075-1729 |
| language | English |
| last_indexed | 2024-03-09T19:56:05Z |
| publishDate | 2022-10-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Life |
| spelling | doaj.art-915e5f4d988847a2a84aba4fa42260de2023-11-24T00:57:12ZengMDPI AGLife2075-17292022-10-011210160510.3390/life12101605Endothelial Dysfunction in COVID-19: Potential Mechanisms and Possible Therapeutic OptionsMaria Chiara Pelle0Isabella Zaffina1Stefania Lucà2Valentina Forte3Vincenzo Trapanese4Melania Melina5Federica Giofrè6Franco Arturi7Unit of Internal Medicine, Department of Medical and Surgical Sciences, University “Magna Graecia” of Catanzaro, 88100 Catanzaro, ItalyUnit of Internal Medicine, Department of Medical and Surgical Sciences, University “Magna Graecia” of Catanzaro, 88100 Catanzaro, ItalyUnit of Internal Medicine, Department of Medical and Surgical Sciences, University “Magna Graecia” of Catanzaro, 88100 Catanzaro, ItalyUnit of Internal Medicine, Department of Medical and Surgical Sciences, University “Magna Graecia” of Catanzaro, 88100 Catanzaro, ItalyUnit of Internal Medicine, Department of Medical and Surgical Sciences, University “Magna Graecia” of Catanzaro, 88100 Catanzaro, ItalyUnit of Internal Medicine, Department of Medical and Surgical Sciences, University “Magna Graecia” of Catanzaro, 88100 Catanzaro, ItalyUnit of Internal Medicine, Department of Medical and Surgical Sciences, University “Magna Graecia” of Catanzaro, 88100 Catanzaro, ItalyUnit of Internal Medicine, Department of Medical and Surgical Sciences, University “Magna Graecia” of Catanzaro, 88100 Catanzaro, ItalySARS-CoV-2, a novel coronavirus found in Wuhan (China) at the end of 2019, is the etiological agent of the current pandemic that is a heterogeneous disease, named coronavirus disease 2019 (COVID-19). SARS-CoV-2 affects primarily the lungs, but it can induce multi-organ involvement such as acute myocardial injury, myocarditis, thromboembolic eventsandrenal failure. Hypertension, chronic kidney disease, diabetes mellitus and obesity increase the risk of severe complications of COVID-19. There is no certain explanation for this systemic COVID-19 involvement, but it could be related to endothelial dysfunction, due to direct (endothelial cells are infected by the virus) and indirect damage (systemic inflammation) factors. Angiotensin-converting enzyme 2 (ACE2), expressed in human endothelium, has a fundamental role in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. In fact, ACE2 is used as a receptor by SARS-CoV-2, leading to the downregulation of these receptors on endothelial cells; once inside, this virus reduces the integrity of endothelial tissue, with exposure of prothrombotic molecules, platelet adhesion, activation of coagulation cascades and, consequently, vascular damage. Systemic microangiopathy and thromboembolism can lead to multi-organ failure with an elevated risk of death. Considering the crucial role of the immunological response and endothelial damage in developing the severe form of COVID-19, in this review, we will attempt to clarify the underlying pathophysiological mechanisms.https://www.mdpi.com/2075-1729/12/10/1605COVID-19SARS-CoV-2inflammationendotheliumpathogenesiscoagulopathy |
| spellingShingle | Maria Chiara Pelle Isabella Zaffina Stefania Lucà Valentina Forte Vincenzo Trapanese Melania Melina Federica Giofrè Franco Arturi Endothelial Dysfunction in COVID-19: Potential Mechanisms and Possible Therapeutic Options Life COVID-19 SARS-CoV-2 inflammation endothelium pathogenesis coagulopathy |
| title | Endothelial Dysfunction in COVID-19: Potential Mechanisms and Possible Therapeutic Options |
| title_full | Endothelial Dysfunction in COVID-19: Potential Mechanisms and Possible Therapeutic Options |
| title_fullStr | Endothelial Dysfunction in COVID-19: Potential Mechanisms and Possible Therapeutic Options |
| title_full_unstemmed | Endothelial Dysfunction in COVID-19: Potential Mechanisms and Possible Therapeutic Options |
| title_short | Endothelial Dysfunction in COVID-19: Potential Mechanisms and Possible Therapeutic Options |
| title_sort | endothelial dysfunction in covid 19 potential mechanisms and possible therapeutic options |
| topic | COVID-19 SARS-CoV-2 inflammation endothelium pathogenesis coagulopathy |
| url | https://www.mdpi.com/2075-1729/12/10/1605 |
| work_keys_str_mv | AT mariachiarapelle endothelialdysfunctionincovid19potentialmechanismsandpossibletherapeuticoptions AT isabellazaffina endothelialdysfunctionincovid19potentialmechanismsandpossibletherapeuticoptions AT stefanialuca endothelialdysfunctionincovid19potentialmechanismsandpossibletherapeuticoptions AT valentinaforte endothelialdysfunctionincovid19potentialmechanismsandpossibletherapeuticoptions AT vincenzotrapanese endothelialdysfunctionincovid19potentialmechanismsandpossibletherapeuticoptions AT melaniamelina endothelialdysfunctionincovid19potentialmechanismsandpossibletherapeuticoptions AT federicagiofre endothelialdysfunctionincovid19potentialmechanismsandpossibletherapeuticoptions AT francoarturi endothelialdysfunctionincovid19potentialmechanismsandpossibletherapeuticoptions |