{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T02:21:05Z","timestamp":1783390865346,"version":"3.54.6"},"reference-count":177,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2022,4,7]],"date-time":"2022-04-07T00:00:00Z","timestamp":1649289600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Lung injury may persist during the recovery period of COVID-19 as shown through imaging, six-minute walk, and lung function tests. The pathophysiological mechanisms leading to long COVID have not been adequately explained. Our aim is to investigate the basis of pulmonary susceptibility during sequelae and the possibility that prothrombotic states may influence long-term pulmonary symptoms of COVID-19. The patient\u2019s lungs remain vulnerable during the recovery stage due to persistent shedding of the virus, the inflammatory environment, the prothrombotic state, and injury and subsequent repair of the blood-air barrier. The transformation of inflammation to proliferation and fibrosis, hypoxia-involved vascular remodeling, vascular endothelial cell damage, phosphatidylserine-involved hypercoagulability, and continuous changes in serological markers all contribute to post-discharge lung injury. Considering the important role of microthrombus and arteriovenous thrombus in the process of pulmonary functional lesions to organic lesions, we further study the possibility that prothrombotic states, including pulmonary vascular endothelial cell activation and hypercoagulability, may affect long-term pulmonary symptoms in long COVID. Early use of combined anticoagulant and antiplatelet therapy is a promising approach to reduce the incidence of pulmonary sequelae. Essentially, early treatment can block the occurrence of thrombotic events. Because impeded pulmonary circulation causes large pressure imbalances over the alveolar membrane leading to the infiltration of plasma into the alveolar cavity, inhibition of thrombotic events can prevent pulmonary hypertension, formation of lung hyaline membranes, and lung consolidation.<\/jats:p>","DOI":"10.3389\/fimmu.2022.862522","type":"journal-article","created":{"date-parts":[[2022,4,7]],"date-time":"2022-04-07T04:57:38Z","timestamp":1649307458000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":43,"title":["Persistent Lung Injury and Prothrombotic State in Long COVID"],"prefix":"10.3389","volume":"13","author":[{"given":"Mengqi","family":"Xiang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haijiao","family":"Jing","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chengyue","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Valerie A.","family":"Novakovic","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jialan","family":"Shi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2022,4,7]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"2001028","DOI":"10.1183\/13993003.01028-2020","article-title":"Clinical Phenotypes of SARS-CoV-2: Implications for Clinicians and Researchers","volume":"55","author":"Rello","year":"2020","journal-title":"Eur Respir J"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.n436","article-title":"Severe COVID-19 Pneumonia: Pathogenesis and Clinical Management","volume":"372","author":"Attaway","year":"2021","journal-title":"BMJ"},{"key":"B3","doi-asserted-by":"publisher","first-page":"1","DOI":"10.1007\/s12016-021-08848-3","article-title":"A Review of Persistent Post-COVID Syndrome (PPCS)","volume":"20","author":"Oronsky","year":"2021","journal-title":"Clin Rev Allergy Immunol"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.cpcardiol.2021.101004","article-title":"Severe Pulmonary Hypertension: An Important Sequel After Severe Post-Acute COVID-19 Pneumonia","volume":"30","author":"Cueto-Robledo","year":"2021","journal-title":"Curr Probl Cardiol"},{"key":"B5","doi-asserted-by":"publisher","first-page":"13","DOI":"10.1016\/j.trsl.2021.09.001","article-title":"From ARDS to Pulmonary Fibrosis: The Next Phase of the COVID-19 Pandemic","volume":"241","author":"Michalski","year":"2022","journal-title":"Transl Res"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.120.047915","article-title":"Differentiating COVID-19 Pneumonia From Acute Respiratory Distress Syndrome and High Altitude Pulmonary Edema: Therapeutic Implications","volume":"142","author":"Archer","year":"2020","journal-title":"Circulation"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1111\/imr.12977","article-title":"COVID-19 and Pulmonary Fibrosis: A Potential Role for Lung Epithelial Cells and Fibroblasts","volume":"302","author":"John","year":"2021","journal-title":"Immunol Rev"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1016\/S2213-2600(20)30243-5","article-title":"Pulmonary and Cardiac Pathology in African American Patients With COVID-19: An Autopsy Series From New Orleans","volume":"8","author":"Fox","year":"2020","journal-title":"Lancet Respir Med"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmi.2021.02.019","article-title":"Pulmonary Long-Term Consequences of COVID-19 Infections After Hospital Discharge","volume":"27","author":"Blanco","year":"2021","journal-title":"Clin Microbiol Infect"},{"key":"B10","doi-asserted-by":"publisher","first-page":"297","DOI":"10.1080\/10408363.2020.1860895","article-title":"COVID-19: From an Acute to Chronic Disease? 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