COVID-19 – A vascular disease
Hasan K Siddiqi 1, Peter Libby 2, Paul M Ridker 1
· 1 Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, United States; Division of Preventive Medicine, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, United States.
· 2 Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, United States. Electronic address: firstname.lastname@example.org.
· PMID: 33068723 PMCID: PMC7556303 DOI: 10.1016/j.tcm.2020.10.005
Free PMC article
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) leads to multi-system dysfunction with emerging evidence suggesting that SARS-CoV-2-mediated endothelial injury is an important effector of the virus. Potential therapies that address vascular system dysfunction and its sequelae may have an important role in treating SARS-CoV-2 infection and its long-lasting effects.
Keywords: Coagulation; Endothelium; Inflammation; Microvessels; Thrombosis.
Conflict of interest statement
Declaration of Competing Interest Hasan Siddiqi: No disclosures Peter Libby: Dr. Libby is an unpaid consultant to, or involved in clinical trials for Amgen, AstraZeneca, Baim Institute, Beren Therapeutics, Esperion, Therapeutics, Genentech, Kancera, Kowa Pharmaceuticals, Medimmune, Merck, Norvo Nordisk, Merck, Novartis, Pfizer, Sanofi-Regeneron. Dr. Libby is a member of scientific advisory board for Amgen, Corvidia Therapeutics, DalCor Pharmaceuticals, Kowa Pharmaceuticals, Olatec Therapeutics, Medimmune, Novartis, XBiotech, Inc. Dr. Libby’s laboratory has received research funding in the last 2 years from Novartis. Dr. Libby is on the Board of Directors of XBiotech, Inc. Dr. Libby has a financial interest in Xbiotech, a company developing therapeutic human antibodies. Dr. Libby’s interests were reviewed and are managed by Brigham and Women’s Hospital and Partners HealthCare in accordance with their conflict of interest policies. Dr. Libby receives funding support from the National Heart, Lung, and Blood Institute (1R01HL134892), the American Heart Association (18CSA34080399), and the RRM Charitable Fund. Paul Ridker: Dr Ridker has received research grant support from Kowa, Novartis, NHLBI, NCI, and Amarin (unrelated to this manuscript) and served as a consultant to Novartis, Jansen, CiviBiopharm, Corvidia, Flame, Agepha, and Inflazome, (unrelated to this manuscript). Dr. Ridker is also part of the National Institutes of Health Accelerating COVID-19 Therapeutic Interventions and Vaccines (ACTIV) collaborative steering committee.
Fig. 1 SARS-CoV-2 Induced Endothelial Injury Legend: A schematic of SARS-CoV-2 infection and proposed resulting endothelial injury, involving immune activation, pro-thrombotic milieu, and RAAS dysregulation. These insults interact with each other to cause end-organ dysfunction that is manifest in many COVID-19 patients. TMPRSS2 = Transmembrane protease serine 2; ADAM17 = A disintegrin and metalloproteinase 17; TNF = Tumor necrosis factor; TNFr = Tumor necrosis factor receptor; TLR = toll-like receptor; DAMPs = Damage-associated molecular patterns; PAMPs = Pathogen-associated molecular patterns; PAI-1 = plasminogen activator inhibitor-1; vWF = von Willebrand factor; eNOS = endothelial nitric oxide; tPA = tissue plasminogen activator; AT1R = angiotensin 1 receptor; ARDS = acute respiratory distress syndrome Created with BioRender.com.