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. 2021 Apr;193(1):43-51.
doi: 10.1111/bjh.17240. Epub 2021 Feb 4.

COVID-19-induced endotheliitis: emerging evidence and possible therapeutic strategies

Eleonora Calabretta  1   2 , Jose M Moraleda  3 , Massimo Iacobelli  4 , Ruben Jara  5 , Israel Vlodavsky  6 , Peter O'Gorman  7 , Antonio Pagliuca  8 , Clifton Mo  9 , Rebecca M Baron  10 , Alessio Aghemo  11   2 , Robert Soiffer  9 , Jawed Fareed  12 , Carmelo Carlo-Stella  1   2 , Paul Richardson  9
Affiliations

COVID-19-induced endotheliitis: emerging evidence and possible therapeutic strategies

Eleonora Calabretta et al. Br J Haematol. 2021 Apr.
No abstract available

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Conflict of interest statement

Jose M. Moraleda declares Advisory Board fees from Jazz Pharmaceuticals; Antonio Pagliuca has received Advisory Board and Speaker fees from Jazz Pharmaceuticals; Rebecca M. Baron is on a Merck Advisory Board and a Consultant for Genentech. Robert Soiffer serves on the Board of Directors for Kiadis and Be The Match/National Marrow Donor Program; provided consulting for Gilead, Rheos Therapeutics, Cugene, Precision Bioscience, Mana Therapeutics, VOR Biopharma, and Novartis; and Data Safety Monitoring Board for Juno/Celgene; Paul Richardson is an Advisory Committee Member for Jazz Pharmaceuticals; Carmelo Carlo‐Stella is a Consultant/Advisory Board Member for Genente Science srl, ADC Therapeutics, Novartis, Roche, Karyopharm, Sanofi, Boehringer Igelheim and Servier. The remaining authors declare nothing to disclose.

Figures

Fig 1
Fig 1
Potential mechanisms of action of defibrotide in the treatment of COVID‐19. Left, defibrotide limits viral attachment by interfering with Syndecan‐1, the primary cell surface heparan sulfate on ECs, and reduces viral dissemination, by inhibiting HPSE‐mediated viral release. Right, effects of defibrotide on endothelial‐mediated pathological processes. Viral infection of ECs promotes apoptosis with breakdown of endothelial barrier and exposure of the subendothelium, with subsequent platelet activation and thrombotic phenomena. Defibrotide inhibits platelet activation and leukocyte recruitment and blocks the generation of the cytokine storm; specifically, HPSE‐mediated activation of immune cells is suppressed, thus limiting the development of cytokine release syndrome. Sars‐Cov‐2, severe acute respiratory syndrome coronavirus‐2; ACE2, angiotensin‐converting enzyme 2; Ang‐2, angiopoietin‐2; GI, gastrointestinal; IL, interleukin; NFKB, nuclear factor kappa‐light chain‐enhancer of activated B cells; TNF‐α, tumor necrosis factor‐alpha; VWF, von Willebrand Factor.
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