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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
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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.

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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

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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)

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