CoChat
Sign Up
Cited by 30

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

Well-Known and Novel Players in Endothelial Dysfunction: Updates on a Notch(ed) Landscape

Fortini, Francesca, Vieceli Dalla Sega, Francesco, Marracino, Luisa, Severi, Paolo, Rapezzi, Claudio, Rizzo, Paola, Ferrari, Roberto·2021·Biomedicines
DOI 10.3390/biomedicines9080997PMC PMC8393382
Open this paper in CoChat — free account

Abstract

Endothelial dysfunction characterizes every aspect of the so-called cardiovascular continuum, a series of events ranging from hypertension to the development of atherosclerosis and, finally, to coronary heart disease, thrombus formation, myocardial infarction, and heart failure. Endothelial dysfunction is the main prognostic factor for the progression of vascular disorders, which responds to drug intervention and lifestyle changes. Virtually all of the drugs used to prevent cardiovascular disorders, such as long-used and new antilipidemic agents and inhibitors of angiotensin enzyme (ACEi), exert an important effect on the endothelium. Endothelial dysfunction is a central feature of coronavirus disease -19 (COVID-19), and it is now clear that life-risk complications of the disease are prompted by alterations of the endothelium induced by viral infection. As a consequence, the progression of COVID-19 is worse in the subjects in whom endothelial dysfunction is already present, such as elderly, diabetic, obese, and hypertensive patients. Importantly, circulating biomarkers of endothelial activation and injury predict the severity and mortality of the disease and can be used to evaluate the efficacy of treatments. The purpose of this review is to provide updates on endothelial function by discussing its clinical relevance in the cardiovascular continuum, the latest insights from molecular and cellular biology, and their implications for clinical practice, with a focus on new actors, such as the Notch signaling and emerging therapies for cardiovascular disease.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.3390/biomedicines9080997

Cites

4 of 4 references verified0 citation errors · 0 not checkable

Statistics

Figures

Figure 1 Opposite effects of ACE inhibitors (ACEi) and angiotensin II receptor blockers (ARBs) on endothelial function. Conversely, ACE inhibition reduces cell death (apoptosis) and extends the lifecycle of endothelial cells. Thus, these drugs maintain endothelial continuity and exert protection against acute coronary syndromes and cardiovascular mortality beyond blood pressure reduction. However, ARBs appear to exert a pro-apoptotic effect on vascular endothelial cells.
Figure 1 Opposite effects of ACE inhibitors (ACEi) and angiotensin II receptor blockers (ARBs) on endothelial function. Conversely, ACE inhibition reduces cell death (apoptosis) and extends the lifecycle of endothelial cells. Thus, these drugs maintain endothelial continuity and exert protection against acute coronary syndromes and cardiovascular mortality beyond blood pressure reduction. However, ARBs appear to exert a pro-apoptotic effect on vascular endothelial cells.CC BY · PubMed Central
Figure 2 Effects of angiotensin II receptor blockers (ARBs). ARBs bind to angiotensin II (Ang II) receptor type 1 (AT1) contrasting vasoconstriction, water retention, promoting proliferation, and limiting apoptosis in the endothelium. When AT1 is inhibited, the circulating Ang II can only bind to the Ang II receptor type 2 (AT2) causing vasodilation, no water retention, reduced proliferation, and increased apoptosis of endothelial cells. In addition, Ang II may also bind to Ang II receptor type 3 and 4 (AT3 and AT4), exerting additional effects that are not fully known yet.
Figure 2 Effects of angiotensin II receptor blockers (ARBs). ARBs bind to angiotensin II (Ang II) receptor type 1 (AT1) contrasting vasoconstriction, water retention, promoting proliferation, and limiting apoptosis in the endothelium. When AT1 is inhibited, the circulating Ang II can only bind to the Ang II receptor type 2 (AT2) causing vasodilation, no water retention, reduced proliferation, and increased apoptosis of endothelial cells. In addition, Ang II may also bind to Ang II receptor type 3 and 4 (AT3 and AT4), exerting additional effects that are not fully known yet.CC BY · PubMed Central
Figure 3 Effects of 48 h incubation of human endothelial umbilical cells (HUVECs) with serum from patients with acute ST-elevation myocardial infarction at entry (within 3 h from symptoms) and 48 h later. Patients were treated with either rosuvastatin 20 mg or perindopril 10 mg. * p < 0.05, different from controls.
Figure 3 Effects of 48 h incubation of human endothelial umbilical cells (HUVECs) with serum from patients with acute ST-elevation myocardial infarction at entry (within 3 h from symptoms) and 48 h later. Patients were treated with either rosuvastatin 20 mg or perindopril 10 mg. * p < 0.05, different from controls.CC BY · PubMed Central
Figure 4 Lipid-mediated and possible direct effects of ANGPTL3 inhibitors on endothelial function. Endothelial dysfunction (ED) is characterized by increased apoptosis, expression of intercellular adhesion molecule (ICAM-1), and impairment of nitric oxide (NO) synthesis. ANGPTL3 inhibitors, such as the antibody Evinacumab and antisense oligonucleotide (ASO), reduce circulating low density lipoproteins (LDL) and triglycerides (TG), hence contrasting lipid-mediated ED. In addition, ANGPTL3 inhibitors may directly protect from ED by impeding the binding of ANGPTL3 to endothelial integrin αvβ3, thus inhibiting the Wnt/β-catenin signaling and restoring protective Notch signaling pathway.
Figure 4 Lipid-mediated and possible direct effects of ANGPTL3 inhibitors on endothelial function. Endothelial dysfunction (ED) is characterized by increased apoptosis, expression of intercellular adhesion molecule (ICAM-1), and impairment of nitric oxide (NO) synthesis. ANGPTL3 inhibitors, such as the antibody Evinacumab and antisense oligonucleotide (ASO), reduce circulating low density lipoproteins (LDL) and triglycerides (TG), hence contrasting lipid-mediated ED. In addition, ANGPTL3 inhibitors may directly protect from ED by impeding the binding of ANGPTL3 to endothelial integrin αvβ3, thus inhibiting the Wnt/β-catenin signaling and restoring protective Notch signaling pathway.CC BY · PubMed Central
Figure 5 Temporal evolution of endothelial biomarkers in COVID-19. Increase of circulating inflammatory cytokines in response to viral infection induces alteration of endothelial cells that can be detected in term of circulating biomarkers. Early-stage inflammation is characterized by increased interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and IL-6; endothelium releases vascular adhesion molecule (VCAM)-1, intercellular adhesion molecule (ICAM)-1, and endoglin in response to inflammation; damaged endothelium releases mediators of coagulation such as thrombomodulin and von Willebrand Factor (vWF).
Figure 5 Temporal evolution of endothelial biomarkers in COVID-19. Increase of circulating inflammatory cytokines in response to viral infection induces alteration of endothelial cells that can be detected in term of circulating biomarkers. Early-stage inflammation is characterized by increased interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and IL-6; endothelium releases vascular adhesion molecule (VCAM)-1, intercellular adhesion molecule (ICAM)-1, and endoglin in response to inflammation; damaged endothelium releases mediators of coagulation such as thrombomodulin and von Willebrand Factor (vWF).CC BY · PubMed Central

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 4 references

Research works printed but not linked: 89

  1. Ferrari, 2010, Secondary prevention of CAD with ACE inhibitors: A struggle between life and death of the endothelium, Cardiovasc. Drugs Ther., 24, 331, 10.1007/s10557-010-6244-x · DOI
  2. Davis, 2004, Shear stress regulates endothelial nitric-oxide synthase promoter activity through nuclear factor kappaB binding, J. Biol. Chem., 279, 163, 10.1074/jbc.M307528200 · DOI
  3. Walpola, 1995, Expression of ICAM-1 and VCAM-1 and monocyte adherence in arteries exposed to altered shear stress, Arterioscler. Thromb. Vasc. Biol., 15, 2, 10.1161/01.ATV.15.1.2 · DOI
  4. Sandoo, 2010, The endothelium and its role in regulating vascular tone, Open Cardiovasc. Med. J., 4, 302, 10.2174/1874192401004010302 · DOI
  5. Cahill, 2016, Vascular endothelium—Gatekeeper of vessel health, Atherosclerosis, 248, 97, 10.1016/j.atherosclerosis.2016.03.007 · DOI · Paper page
  6. Mollace, 2015, Oxidized LDL attenuates protective autophagy and induces apoptotic cell death of endothelial cells: Role of oxidative stress and LOX-1 receptor expression, Int. J. Cardiol., 184, 152, 10.1016/j.ijcard.2015.02.007 · DOI
  7. Aquila, 2017, Context-dependent function of ROS in the vascular endothelium: The role of the Notch pathway and shear stress, Biofactors, 43, 475, 10.1002/biof.1359 · DOI
  8. Aquila, 2018, Heart rate reduction with ivabradine in the early phase of atherosclerosis is protective in the endothelium of ApoE-deficient mice, J. Physiol. Pharmacol., 69, 35
  9. Fortini, 2019, Notch signaling regulates immune responses in atherosclerosis, Front. Immunol., 10, 1130, 10.3389/fimmu.2019.01130 · DOI
  10. Souilhol, 2020, Endothelial responses to shear stress in atherosclerosis: A novel role for developmental genes, Nat. Rev. Cardiol., 17, 52, 10.1038/s41569-019-0239-5 · DOI
  11. Caliceti, 2014, ROS, Notch, and Wnt signaling pathways: Crosstalk between three major regulators of cardiovascular biology, BioMed Res. Int., 2014, 318714, 10.1155/2014/318714 · DOI
  12. Chapouly, 2020, Desert hedgehog-driven endothelium integrity is enhanced by gas1 (growth arrest-specific 1) but negatively regulated by Cdon (cell adhesion molecule-related/downregulated by oncogenes), Arterioscler. Thromb. Vasc. Biol., 40, e336, 10.1161/ATVBAHA.120.314441 · DOI
  13. Boopathy, 2019, Role of hippo pathway-YAP/TAZ signaling in angiogenesis, Front. Cell Dev. Biol., 7, 49, 10.3389/fcell.2019.00049 · DOI
  14. Libby, 2020, COVID-19 is, in the end, an endothelial disease, Eur. Heart J., 41, 3038, 10.1093/eurheartj/ehaa623 · DOI
  15. Alexander, 2021, Endothelial function in cardiovascular medicine: A consensus paper of the European Society of Cardiology Working Groups on Atherosclerosis and Vascular Biology, Aorta and Peripheral Vascular Diseases, Coronary Pathophysiology and Microcirculation, and Thrombosis, Cardiovasc. Res., 117, 29, 10.1093/cvr/cvaa085 · DOI
  16. Lee, 2018, Effects of Statins on Coronary Atherosclerotic Plaques: The PARADIGM Study, JACC Cardiovasc. Imaging, 11, 1475, 10.1016/j.jcmg.2018.04.015 · DOI
  17. Landgraf, 2002, ACE inhibition and atherogenesis, Can. J. Physiol. Pharmacol., 80, 354, 10.1139/y02-038 · DOI
  18. Rizzo, 2013, The Notch pathway: A crossroad between the life and death of the endothelium, Eur. Heart J., 34, 2504, 10.1093/eurheartj/ehs141 · DOI
  19. Aquila, 2019, The Notch pathway: A novel therapeutic target for cardiovascular diseases?, Expert Opin. Ther. Targets, 23, 695, 10.1080/14728222.2019.1641198 · DOI
  20. Mack, 2017, NOTCH1 is a mechanosensor in adult arteries, Nat. Commun., 8, 1620, 10.1038/s41467-017-01741-8 · DOI
  21. Theodoris, 2015, Human disease modeling reveals integrated transcriptional and epigenetic mechanisms of NOTCH1 haploinsufficiency, Cell, 160, 1072, 10.1016/j.cell.2015.02.035 · DOI · Paper page
  22. Quillard, 2010, Inflammation dysregulates Notch signaling in endothelial cells: Implication of Notch2 and Notch4 to endothelial dysfunction, Biochem. Pharmacol., 80, 2032, 10.1016/j.bcp.2010.07.010 · DOI
  23. Fortini, 2017, Estrogen receptor β-dependent Notch1 activation protects vascular endothelium against tumor necrosis factor α (TNFα)-induced apoptosis, J. Biol. Chem., 292, 18178, 10.1074/jbc.M117.790121 · DOI
  24. Fortini, 2019, Estrogen-mediated protection against coronary heart disease: The role of the Notch pathway, J. Steroid Biochem. Mol. Biol., 189, 87, 10.1016/j.jsbmb.2019.02.008 · DOI
  25. Quillard, 2008, Impaired Notch4 activity elicits endothelial cell activation and apoptosis: Implication for transplant arteriosclerosis, Arterioscler. Thromb. Vasc. Biol., 28, 2258, 10.1161/ATVBAHA.108.174995 · DOI
  26. Polacheck, 2017, A non-canonical Notch complex regulates adherens junctions and vascular barrier function, Nature, 552, 258, 10.1038/nature24998 · DOI
  27. Vieceli Dalla Sega, F., Mastrocola, R., Aquila, G., Fortini, F., Fornelli, C., Zotta, A., Cento, A.S., Perrelli, A., Boda, E., and Pannuti, A. (2019). KRIT1 Deficiency Promotes Aortic Endothelial Dysfunction. Int. J. Mol. Sci., 20. · DOI
  28. Briot, 2015, Endothelial NOTCH1 is suppressed by circulating lipids and antagonizes inflammation during atherosclerosis, J. Exp. Med., 212, 2147, 10.1084/jem.20150603 · DOI
  29. Caliceti, C., Aquila, G., Pannella, M., Morelli, M.B., Fortini, C., Pinton, P., Bonora, M., Hrelia, S., Pannuti, A., and Miele, L. (2013). 17β-estradiol enhances signalling mediated by VEGF-A-delta-like ligand 4-notch1 axis in human endothelial cells. PLoS ONE, 8. · DOI
  30. Norum, 2016, Increased serum levels of the notch ligand DLL1 are associated with diastolic dysfunction, reduced exercise capacity, and adverse outcome in chronic heart failure, J. Card. Fail., 22, 218, 10.1016/j.cardfail.2015.07.012 · DOI
  31. Rizzo, 2020, COVID-19 in the heart and the lungs: Could we “Notch” the inflammatory storm?, Basic Res. Cardiol., 115, 31, 10.1007/s00395-020-0791-5 · DOI
  32. Breikaa, 2021, The Notch Pathway: A Link between COVID-19 Pathophysiology and Its Cardiovascular Complications, Front. Cardiovasc. Med., 8, 681948, 10.3389/fcvm.2021.681948 · DOI
  33. Iaconelli, 2020, First detection of SARS-CoV-2 in untreated wastewaters in Italy, Sci. Total Environ., 736, 139652, 10.1016/j.scitotenv.2020.139652 · DOI
  34. Vandelli, 2020, Structural analysis of SARS-CoV-2 genome and predictions of the human interactome, Nucleic Acids Res., 48, 11270, 10.1093/nar/gkaa864 · DOI
  35. Harb, 2021, Notch4 signaling limits regulatory T-cell-mediated tissue repair and promotes severe lung inflammation in viral infections, Immunity, 54, 1186, 10.1016/j.immuni.2021.04.002 · DOI
  36. Cangiano, 2011, ACE inhibition modulates endothelial apoptosis and renewal via endothelial progenitor cells in patients with acute coronary syndromes, Am. J. Cardiovasc. Drugs, 11, 189, 10.2165/11589400-000000000-00000 · DOI
  37. Ferrari, 2014, Coronary artery disease: Use of ACE inhibitors in stable CAD—what is the truth?, Nat. Rev. Cardiol., 11, 315, 10.1038/nrcardio.2014.56 · DOI
  38. Agnoletti, 1999, Serum from patients with severe heart failure downregulates eNOS and is proapoptotic: Role of tumor necrosis factor-alpha, Circulation, 100, 1983, 10.1161/01.CIR.100.19.1983 · DOI
  39. Valgimigli, 2003, Serum from patients with acute coronary syndromes displays a proapoptotic effect on human endothelial cells: A possible link to pan-coronary syndromes, Circulation, 107, 264, 10.1161/01.CIR.0000045665.57256.86 · DOI
  40. Bachetti, 1998, Effects of chronic noradrenaline on the nitric oxide pathway in human endothelial cells, Basic Res. Cardiol., 93, 250, 10.1007/s003950050092 · DOI
  41. Ceconi, 2007, Differences in the effect of angiotensin-converting enzyme inhibitors on the rate of endothelial cell apoptosis: In vitro and in vivo studies, Cardiovasc. Drugs Ther., 21, 423, 10.1007/s10557-007-6068-5 · DOI
  42. Strauss, 2006, Angiotensin receptor blockers may increase risk of myocardial infarction: Unraveling the ARB-MI paradox, Circulation, 114, 838, 10.1161/CIRCULATIONAHA.105.594986 · DOI
  43. Ferrari, 2013, The impact of ACE inhibition on all-cause and cardiovascular mortality in contemporary hypertension trials: A review, Expert Rev. Cardiovasc. Ther., 11, 705, 10.1586/erc.13.42 · DOI
  44. Bangalore, 2016, Angiotensin-converting enzyme inhibitors or angiotensin receptor blockers in patients without heart failure? Insights from 254,301 patients from randomized trials, Mayo Clin. Proc., 91, 51, 10.1016/j.mayocp.2015.10.019 · DOI
  45. Savarese, 2013, A meta-analysis reporting effects of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in patients without heart failure, J. Am. Coll. Cardiol., 61, 131, 10.1016/j.jacc.2012.10.011 · DOI
  46. Cheng, 2014, Effect of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on all-cause mortality, cardiovascular deaths, and cardiovascular events in patients with diabetes mellitus: A meta-analysis, JAMA Intern. Med., 174, 773, 10.1001/jamainternmed.2014.348 · DOI
  47. Thomopoulos, 2015, Effects of blood pressure lowering on outcome incidence in hypertension: 4. Effects of various classes of antihypertensive drugs--overview and meta-analyses, J. Hypertens., 33, 195, 10.1097/HJH.0000000000000447 · DOI
  48. Messerli, 2017, Angiotensin receptor blockers reduce cardiovascular events, including the risk of myocardial infarction, Circulation, 135, 2085, 10.1161/CIRCULATIONAHA.116.025950 · DOI
  49. Strauss, 2017, Angiotensin receptor blockers do not reduce risk of myocardial infarction, cardiovascular death, or total mortality: Further evidence for the ARB-MI paradox, Circulation, 135, 2088, 10.1161/CIRCULATIONAHA.117.026112 · DOI
  50. Ceconi, 2007, ACE inhibition with perindopril and endothelial function. Results of a substudy of the EUROPA study: PERTINENT, Cardiovasc. Res., 73, 237, 10.1016/j.cardiores.2006.10.021 · DOI
  51. Agnoletti, 2007, Rosuvastatin stimulates eNOS and inhibits apoptosis in HUVECs exposed to sera from cardiovascular diseases patients, J. Mol. Cell. Cardiol., 42, S226, 10.1016/j.yjmcc.2007.03.681 · DOI
  52. Zacharek, 2009, Simvastatin increases notch signaling activity and promotes arteriogenesis after stroke, Stroke, 40, 254, 10.1161/STROKEAHA.108.524116 · DOI · Paper page
  53. Musunuru, 2010, Exome sequencing, ANGPTL3 mutations, and familial combined hypolipidemia, N. Engl. J. Med., 363, 2220, 10.1056/NEJMoa1002926 · DOI · Paper page
  54. Xu, 2018, Role of angiopoietin-like 3 (ANGPTL3) in regulating plasma level of low-density lipoprotein cholesterol, Atherosclerosis, 268, 196, 10.1016/j.atherosclerosis.2017.08.031 · DOI · Paper page
  55. Camenisch, 2002, ANGPTL3 stimulates endothelial cell adhesion and migration via integrin alpha vbeta 3 and induces blood vessel formation in vivo, J. Biol. Chem., 277, 17281, 10.1074/jbc.M109768200 · DOI
  56. Yi, 2016, Integrin alphavbeta3 enhances β-catenin signaling in acute myeloid leukemia harboring Fms-like tyrosine kinase-3 internal tandem duplication mutations: Implications for microenvironment influence on sorafenib sensitivity, Oncotarget, 7, 40387, 10.18632/oncotarget.9617 · DOI
  57. Zheng, 2018, Glycogen synthase kinase 3β inhibition enhances Notch1 recycling, Mol. Biol. Cell, 29, 389, 10.1091/mbc.E17-07-0474 · DOI
  58. Herrmann, 2006, Angiogenesis in atherogenesis, Arterioscler. Thromb. Vasc. Biol., 26, 1948, 10.1161/01.ATV.0000233387.90257.9b · DOI
  59. Perico, 2021, Immunity, endothelial injury and complement-induced coagulopathy in COVID-19, Nat. Rev. Nephrol., 17, 46, 10.1038/s41581-020-00357-4 · DOI
  60. Hamming, 2004, Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis, J. Pathol., 203, 631, 10.1002/path.1570 · DOI · Paper page
  61. Monteil, 2020, Inhibition of SARS-CoV-2 infections in engineered human tissues using clinical-grade soluble human ACE2, Cell, 181, 905, 10.1016/j.cell.2020.04.004 · DOI · Paper page
  62. Ackermann, 2020, Pulmonary vascular endothelialitis, thrombosis, and angiogenesis in COVID-19, N. Engl. J. Med., 383, 120, 10.1056/NEJMoa2015432 · DOI · Paper page
  63. Varga, 2020, Endothelial cell infection and endotheliitis in COVID-19, Lancet, 395, 1417, 10.1016/S0140-6736(20)30937-5 · DOI · Paper page
  64. Bryce, 2020, Central nervous system involvement by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), J. Med. Virol., 92, 699, 10.1002/jmv.25915 · DOI · Paper page
  65. Colmenero, 2020, SARS-CoV-2 endothelial infection causes COVID-19 chilblains: Histopathological, immunohistochemical and ultrastructural study of seven paediatric cases, Br. J. Dermatol., 183, 729, 10.1111/bjd.19327 · DOI
  66. Goldsmith, 2020, Electron microscopy of SARS-CoV-2: A challenging task, Lancet, 395, e99, 10.1016/S0140-6736(20)31188-0 · DOI
  67. Dittmayer, 2020, Why misinterpretation of electron micrographs in SARS-CoV-2-infected tissue goes viral, Lancet, 396, e64, 10.1016/S0140-6736(20)32079-1 · DOI
  68. Schaefer, 2020, In situ detection of SARS-CoV-2 in lungs and airways of patients with COVID-19, Mod. Pathol., 33, 2104, 10.1038/s41379-020-0595-z · DOI
  69. Ahmetaj-Shala, B., Peacock, T.P., Baillon, L., Swann, O.C., Gashaw, H., Barclay, W.S., and Mitchell, J.A. (2020). Resistance of endothelial cells to SARS-CoV-2 infection in vitro. bioRxiv. · DOI
  70. Liu, 2021, SARS-CoV-2 Infects Endothelial Cells, Front. Cell Infect. Microbiol., 11, 701278, 10.3389/fcimb.2021.701278 · DOI
  71. Teuwen, 2020, COVID-19: The vasculature unleashed, Nat. Rev. Immunol., 20, 389, 10.1038/s41577-020-0343-0 · DOI
  72. Rauch, 2020, Endotheliopathy is induced by plasma from critically ill patients and associated with organ failure in severe COVID-19, Circulation, 142, 1881, 10.1161/CIRCULATIONAHA.120.050907 · DOI
  73. Canzano, 2021, Platelet and endothelial activation as potential mechanisms behind the thrombotic complications of COVID-19 patients, JACC Basic Transl. Sci., 6, 202, 10.1016/j.jacbts.2020.12.009 · DOI
  74. Campo, 2021, Over time relationship between platelet reactivity, myocardial injury and mortality in patients with SARS-CoV-2-associated respiratory failure, Platelets., 32, 560, 10.1080/09537104.2020.1852543 · DOI
  75. Evans, 2020, Endothelial dysfunction in COVID-19: A position paper of the ESC Working Group for Atherosclerosis and Vascular Biology, and the ESC Council of Basic Cardiovascular Science, Cardiovasc. Res., 116, 2177, 10.1093/cvr/cvaa230 · DOI
  76. Bonaventura, 2018, The pathophysiological role of neutrophil extracellular traps in inflammatory diseases, Thromb. Haemost., 118, 6, 10.1160/TH17-09-0630 · DOI
  77. Radermecker, 2020, Neutrophil extracellular traps infiltrate the lung airway, interstitial, and vascular compartments in severe COVID-19, J. Exp. Med., 217, e20201012, 10.1084/jem.20201012 · DOI
  78. Dupont, 2021, Vascular endothelial damage in the pathogenesis of organ injury in severe COVID-19, Arterioscler. Thromb. Vasc. Biol., 41, 1760, 10.1161/ATVBAHA.120.315595 · DOI
  79. Fortini, 2021, Time course of endothelial dysfunction markers and mortality in COVID-19 patients: A pilot study, Clin. Transl. Med., 11, e283, 10.1002/ctm2.283 · DOI
  80. Spadaro, 2021, Markers of endothelial and epithelial pulmonary injury in mechanically ventilated COVID-19 ICU patients, Crit. Care, 25, 74, 10.1186/s13054-021-03499-4 · DOI
  81. Goshua, 2020, Endotheliopathy in COVID-19-associated coagulopathy: Evidence from a single-centre, cross-sectional study, Lancet Haematol., 7, e575, 10.1016/S2352-3026(20)30216-7 · DOI
  82. Smadja, 2020, Angiopoietin-2 as a marker of endothelial activation is a good predictor factor for intensive care unit admission of COVID-19 patients, Angiogenesis, 23, 611, 10.1007/s10456-020-09730-0 · DOI
  83. Guervilly, 2020, Circulating Endothelial Cells as a Marker of Endothelial Injury in Severe COVID-19, J. Infect. Dis., 222, 1789, 10.1093/infdis/jiaa528 · DOI
  84. Campo, 2017, Biological effects of ticagrelor over clopidogrel in patients with stable coronary artery disease and chronic obstructive pulmonary disease, Thromb. Haemost., 117, 1208, 10.1160/TH16-12-0973 · DOI
  85. Nagashima, 2020, Endothelial Dysfunction and Thrombosis in Patients With COVID-19-Brief Report, Arterioscler. Thromb. Vasc. Biol., 40, 2404, 10.1161/ATVBAHA.120.314860 · DOI
  86. Swanson, 2019, The NLRP3 inflammasome: Molecular activation and regulation to therapeutics, Nat. Rev. Immunol., 19, 477, 10.1038/s41577-019-0165-0 · DOI · Paper page
  87. Rodrigues, 2021, Inflammasomes are activated in response to SARS-CoV-2 infection and are associated with COVID-19 severity in patients, J. Exp. Med., 218, e20201707, 10.1084/jem.20201707 · DOI · Paper page
  88. Jia, 2019, Endothelial cell pyroptosis plays an important role in Kawasaki disease via HMGB1/RAGE/cathespin B signaling pathway and NLRP3 inflammasome activation, Cell Death. Dis., 10, 778, 10.1038/s41419-019-2021-3 · DOI
  89. Mitra, 2018, Microparticulate Caspase 1 Regulates Gasdermin D and Pulmonary Vascular Endothelial Cell Injury, Am. J. Respir. Cell Mol. Biol., 59, 56, 10.1165/rcmb.2017-0393OC · DOI

Cited by

Sorted by citations

Metadata

Authors
Fortini, F., Vieceli Dalla Sega, F., Marracino, L., Severi, P., Rapezzi, C., Rizzo, P., & Ferrari, R.
Affiliations
  • Maria Cecilia Hospital, GVM Care & Research, 48033 Cotignola, Italy
  • Laboratory for Technologies of Advanced Therapies (LTTA), Department of Translational Medicine, University of Ferrara, 44121 Ferrara, Italy
ORCID
Venue
Biomedicines
Publisher
MDPI AG
Published
2021-08-11
Volume
9
Issue
8
Pages
997
ISSN
2227-9059
DOI
10.3390/biomedicines9080997
PMC
PMC8393382
Cited by
30
References
4
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review