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Article ; Online: Arterial Stiffness: From Basic Primers to Integrative Physiology.

Regnault, Véronique / Lacolley, Patrick / Laurent, Stéphane

2023 Volume 86, Page(s) 99–121

Abstract: The elastic properties of conductance arteries are one of the most important hemodynamic functions in the body, and data continue to emerge regarding the importance of their dysfunction in vascular aging and a range of cardiovascular diseases. Here, we ... ...

Abstract	The elastic properties of conductance arteries are one of the most important hemodynamic functions in the body, and data continue to emerge regarding the importance of their dysfunction in vascular aging and a range of cardiovascular diseases. Here, we provide new insight into the integrative physiology of arterial stiffening and its clinical consequence. We also comprehensively review progress made on pathways/molecules that appear today as important basic determinants of arterial stiffness, particularly those mediating the vascular smooth muscle cell (VSMC) contractility, plasticity and stiffness. We focus on membrane and nuclear mechanotransduction, clearance function of the vascular wall, phenotypic switching of VSMCs, immunoinflammatory stimuli and epigenetic mechanisms. Finally, we discuss the most important advances of the latest clinical studies that revisit the classical therapeutic concepts of arterial stiffness and lead to a patient-by-patient strategy according to cardiovascular risk exposure and underlying disease.
MeSH term(s)	Humans ; Vascular Stiffness ; Mechanotransduction, Cellular ; Arteries/metabolism ; Cardiovascular Diseases/metabolism ; Aging/metabolism
Language	English
Publishing date	2023-01-20
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	207933-1
ISSN	1545-1585 ; 0066-4278
ISSN (online)	1545-1585
ISSN	0066-4278
DOI	10.1146/annurev-physiol-042022-031925
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Article ; Online: Conductance Artery Wall Layers and Their Respective Roles in the Clearance Functions.

Michel, Jean-Baptiste / Lagrange, Jeremy / Regnault, Veronique / Lacolley, Patrick

Arteriosclerosis, thrombosis, and vascular biology

2022 Volume 42, Issue 9, Page(s) e253–e272

Abstract: Evolutionary organization of the arterial wall into layers occurred concomitantly with the emergence of a highly muscularized, pressurized arterial system that facilitates outward hydraulic conductance and mass transport of soluble substances across the ... ...

Abstract	Evolutionary organization of the arterial wall into layers occurred concomitantly with the emergence of a highly muscularized, pressurized arterial system that facilitates outward hydraulic conductance and mass transport of soluble substances across the arterial wall. Although colliding circulating cells disperse potential energy within the arterial wall, the different layers counteract this effect: (1) the endothelium ensures a partial barrier function; (2) the media comprises smooth muscle cells capable of endocytosis/phagocytosis; (3) the outer adventitia and perivascular adipocytic tissue are the final receptacles of convected substances. While the endothelium forms a physical and a biochemical barrier, the medial layer is avascular, relying on the specific permeability properties of the endothelium for metabolic support. Different components of the media interact with convected molecules: medial smooth muscle cells take up numerous molecules via scavenger receptors and are capable of phagocytosis of macro/micro particles. The outer layers-the highly microvascularized innervated adventitia and perivascular adipose tissue-are also involved in the clearance functions of the media: the adventitia is the seat of immune response development, inward angiogenesis, macromolecular lymphatic drainage, and neuronal stimulation. Consequently, the clearance functions of the arterial wall are physiologically essential, but also may favor the development of arterial wall pathologies. This review describes how the walls of large conductance arteries have acquired physiological clearance functions, how this is determined by the attributes of the endothelial barrier, governed by endocytic and phagocytic capacities of smooth muscle cells, impacting adventitial functions, and the role of these clearance functions in arterial wall diseases.
MeSH term(s)	Adipose Tissue ; Adventitia/pathology ; Arteries/pathology ; Humans ; Myocytes, Smooth Muscle/pathology ; Vascular Diseases/pathology
Language	English
Publishing date	2022-08-04
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.122.317759
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Zs.A 1705: Show issues

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Article ; Online: Alpha-2-macroglobulin in hemostasis and thrombosis: An underestimated old double-edged sword.

Lagrange, Jeremy / Lecompte, Thomas / Knopp, Tanja / Lacolley, Patrick / Regnault, Véronique

Journal of thrombosis and haemostasis : JTH

2022 Volume 20, Issue 4, Page(s) 806–815

Abstract: Antiproteinases such as alpha-2-macroglobulin (A2M) play a role in hemostasis. A2M is highly conserved throughout evolution and is a high molecular weight homo-tetrameric glycoprotein. A2M proteinase inhibitor activity is possible via a unique cage ... ...

Abstract	Antiproteinases such as alpha-2-macroglobulin (A2M) play a role in hemostasis. A2M is highly conserved throughout evolution and is a high molecular weight homo-tetrameric glycoprotein. A2M proteinase inhibitor activity is possible via a unique cage structure leading to proteinase entrapment without direct enzymatic activity inhibition. Following this entrapment, proteinase clearance is possible through A2M binding to the low-density lipoprotein receptor-related protein 1. A2M synthesis is regulated by pro-inflammatory cytokines and increases during several chronic or acute inflammatory diseases and varies with age. For instance, A2M plasma levels are known to be increased in patients with diabetes mellitus, nephrotic syndrome, or sepsis. Concerning hemostasis, A2M can trap many proteinases involved in coagulation and fibrinolysis. Because of its pleiotropic effects A2M can be seen as both anti- and pro-hemostatic. A2M can inhibit thrombin, factor Xa, activated protein C, plasmin, tissue-plasminogen activator, and urokinase. Through its many different functions A2M is generally put apart in the balanced regulation of hemostasis. In addition, the fact that A2M plasma levels are differently regulated during inflammatory-related diseases and that A2M can neutralize cytokines that also modify hemostasis could explain why it is difficult to link common proteins and parameters of hemostasis with the mechanisms of thrombosis in such diseases. Thus, we propose in the present review to summarize known functions of A2M, give a brief overview about diseases, and then to focus on the roles of this antiproteinase in hemostasis and thrombosis.
MeSH term(s)	Cytokines ; Female ; Hemostasis ; Humans ; Pregnancy ; Pregnancy-Associated alpha 2-Macroglobulins ; Thrombin ; Thrombosis ; Transcription Factors ; alpha-Macroglobulins/metabolism
Chemical Substances	Cytokines ; Pregnancy-Associated alpha 2-Macroglobulins ; Transcription Factors ; alpha-Macroglobulins ; Thrombin (EC 3.4.21.5)
Language	English
Publishing date	2022-01-30
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2112661-6
ISSN	1538-7836 ; 1538-7933
ISSN (online)	1538-7836
ISSN	1538-7933
DOI	10.1111/jth.15647
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Zs.A 5805: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 295: Show issues

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Article ; Online: Smooth Muscle Cell Molecular Underpinnings of Vascular Ageing.

Regnault, Veronique / Raoul, Alexandre / Schellenberg, Celia / Lacolley, Patrick

Heart, lung & circulation

2021 Volume 30, Issue 11, Page(s) 1595–1598

MeSH term(s)	Muscle, Smooth, Vascular ; Myocytes, Smooth Muscle ; Vascular Stiffness
Language	English
Publishing date	2021-10-01
Publishing country	Australia
Document type	Editorial
ZDB-ID	2020980-0
ISSN	1444-2892 ; 1443-9506
ISSN (online)	1444-2892
ISSN	1443-9506
DOI	10.1016/j.hlc.2021.09.002
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Article ; Online: Mechanisms of Arterial Stiffening: From Mechanotransduction to Epigenetics.

Lacolley, Patrick / Regnault, Véronique / Laurent, Stéphane

Arteriosclerosis, thrombosis, and vascular biology

2020 Volume 40, Issue 5, Page(s) 1055–1062

Abstract: Arterial stiffness is a major independent risk factor for cardiovascular complications causing isolated systolic hypertension and increased pulse pressure in the microvasculature of target organs. Stiffening of the arterial wall is determined by common ... ...

Abstract	Arterial stiffness is a major independent risk factor for cardiovascular complications causing isolated systolic hypertension and increased pulse pressure in the microvasculature of target organs. Stiffening of the arterial wall is determined by common mechanisms including reduced elastin/collagen ratio, production of elastin cross-linking, reactive oxygen species-induced inflammation, calcification, vascular smooth muscle cell stiffness, and endothelial dysfunction. This brief review will discuss current biological mechanisms by which other cardiovascular risk factors (eg, aging, hypertension, diabetes mellitus, and chronic kidney disease) cause arterial stiffness, with a particular focus on recent advances regarding nuclear mechanotransduction, mitochondrial oxidative stress, metabolism and dyslipidemia, genome mutations, and epigenetics. Targeting these different molecular pathways at different time of cardiovascular risk factor exposure may be a novel approach for discovering drugs to reduce arterial stiffening without affecting artery strength and normal remodeling.
MeSH term(s)	Animals ; Arteries/metabolism ; Arteries/physiopathology ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/genetics ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/physiopathology ; Comorbidity ; Energy Metabolism ; Epigenesis, Genetic ; Humans ; Mechanotransduction, Cellular ; Oxidative Stress ; Risk Assessment ; Risk Factors ; Vascular Stiffness
Language	English
Publishing date	2020-02-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.119.313129
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Article ; Online: Sex Differences in Arterial Stiffening and Central Pulse Pressure: Mechanistic Insights?

Safar, Michel E / Regnault, Véronique / Lacolley, Patrick

Journal of the American College of Cardiology

2020 Volume 75, Issue 8, Page(s) 881–883

MeSH term(s)	Arteries ; Blood Pressure ; Female ; Humans ; Male ; Sex Characteristics ; Vascular Stiffness
Language	English
Publishing date	2020-03-04
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	605507-2
ISSN	1558-3597 ; 0735-1097
ISSN (online)	1558-3597
ISSN	0735-1097
DOI	10.1016/j.jacc.2019.12.041
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Zs.A 1846: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 196: Show issues

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Article ; Online: Thrombin generation on vascular cells in the presence of factor VIII and/or emicizumab.

Atsou, Sénadé / Schellenberg, Célia / Lagrange, Jeremy / Lacolley, Patrick / Lenting, Peter J / Denis, Cécile V / Christophe, Olivier D / Regnault, Véronique

Journal of thrombosis and haemostasis : JTH

2023 Volume 22, Issue 1, Page(s) 112–125

Abstract: Background: The effect of factor VIII (FVIII) or emicizumab on thrombin generation is usually assessed in assays using synthetic phospholipids. Here, we assessed thrombin generation at the surface of human arterial cells (aortic endothelial cells [hAECs] ...

Abstract	Background: The effect of factor VIII (FVIII) or emicizumab on thrombin generation is usually assessed in assays using synthetic phospholipids. Here, we assessed thrombin generation at the surface of human arterial cells (aortic endothelial cells [hAECs] and aortic vascular smooth muscle cells [hVSMCs]). Objectives: To explore the capacity of hAECs (resting or stimulated) and hVSMCs to support thrombin generation by FVIII or emicizumab. Methods: Primary hVSMCs and hAECs were analyzed for tissue factor (TF)-activity and antigen, phosphatidylserine (PS)-exposure, tissue factor pathway inhibitor (TFPI)-content and thrombomodulin expression. Cells were incubated with FVIII-deficient plasma spiked with FVIII, emicizumab, activated prothrombin complex concentrate (APCC) or combinations thereof. Results: TF activity and PS-exposure were present on both hVSMCs and hAECs. In contrast, thrombomodulin and TFPI were expressed on hAECs, while virtually lacking on hVSMCs, confirming the procoagulant nature of hVSMCs. Tumor necrosis factor α-mediated stimulation of hAECs increased not only TF antigen, TF activity, and PS-exposure but also TFPI and thrombomodulin expression. As expected, FVIII and emicizumab promoted thrombin generation on nonstimulated hAECs and hVSMCs, with more thrombin being generated on hVSMCs. Unexpectedly, FVIII and emicizumab increased thrombin generation to a lesser extent on stimulated hAECs compared with nonstimulated hAECs. Finally, adding emicizumab to FVIII did not further increase thrombin generation, whereas the addition of emicizumab to APCC resulted in exaggerated thrombin generation. Conclusion: Tumor necrosis factor stimulation of hAECs increases both pro- and anticoagulant activity. Unexpectedly, the increased anticoagulant activity is sufficient to limit both FVIII- and emicizumab-induced thrombin generation. This protective effect disappears when emicizumab is combined with APCC.
MeSH term(s)	Humans ; Factor VIII/metabolism ; Thrombin/metabolism ; Thrombomodulin ; Endothelial Cells/metabolism ; Hemostatics ; Antibodies, Bispecific/pharmacology ; Factor VIIa ; Factor IX ; Anticoagulants ; Hemophilia A
Chemical Substances	Factor VIII (9001-27-8) ; Thrombin (EC 3.4.21.5) ; emicizumab (7NL2E3F6K3) ; Thrombomodulin ; Hemostatics ; Antibodies, Bispecific ; Factor VIIa (EC 3.4.21.21) ; Factor IX (9001-28-9) ; Anticoagulants
Language	English
Publishing date	2023-09-29
Publishing country	England
Document type	Journal Article
ZDB-ID	2112661-6
ISSN	1538-7836 ; 1538-7933
ISSN (online)	1538-7836
ISSN	1538-7933
DOI	10.1016/j.jtha.2023.09.017
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Zs.A 5805: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 295: Show issues

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Article ; Online: Sirtuin 1 steers anti-inflammatory effects in vascular smooth muscle cells: protection without burden?

Regnault, Véronique / Lacolley, Patrick

Cardiovascular research

2017 Volume 113, Issue 10, Page(s) 1096–1098

MeSH term(s)	Anti-Inflammatory Agents ; Cells, Cultured ; Muscle, Smooth, Vascular ; Myocytes, Smooth Muscle ; Sirtuin 1
Chemical Substances	Anti-Inflammatory Agents ; Sirtuin 1 (EC 3.5.1.-)
Language	English
Publishing date	2017-09-12
Publishing country	England
Document type	Editorial ; Comment
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvx131
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Zs.A 565: Show issues

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Article ; Online: Long-term follow-up of neutrophil activation after severe-to-critical SARS-CoV-2 infection: A longitudinal study.

Valentin, Simon / Regnault, Veronique / Gueant, Jean-Louis / Ribeiro Baptista, Bruno / Abel, Thery / Lacolley, Patrick / Schlemmer, Frederic / Chaouat, Ari / Chabot, François / Gueant-Rodriguez, Rosa-Maria

Allergy

2024

Language	English
Publishing date	2024-04-12
Publishing country	Denmark
Document type	Journal Article
ZDB-ID	391933-x
ISSN	1398-9995 ; 0105-4538
ISSN (online)	1398-9995
ISSN	0105-4538
DOI	10.1111/all.16123
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Zs.MO 125: Show issues

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Article ; Online: Arterial Stiffness in Hypertension and Function of Large Arteries.

Zhang, Yi / Lacolley, Patrick / Protogerou, Athanase D / Safar, Michel E

American journal of hypertension

2020 Volume 33, Issue 4, Page(s) 291–296

Abstract: Background: Arterial stiffness-typically assessed from non-invasive measurement of pulse wave velocity along a straight portion of the vascular tree between the right common carotid and femoral arteries-is a reliable predictor of cardiovascular risk in ... ...

Abstract	Background: Arterial stiffness-typically assessed from non-invasive measurement of pulse wave velocity along a straight portion of the vascular tree between the right common carotid and femoral arteries-is a reliable predictor of cardiovascular risk in patients with essential hypertension. Methods: We reviewed how carotid-femoral pulse wave velocity increases with age and is significantly higher in hypertension (than in age- and gender-matched individuals without hypertension), particularly when hypertension is associated with diabetes mellitus. Results: From the elastic aorta to the muscular peripheral arteries of young healthy individuals, there is a gradual but significant increase in stiffness, with a specific gradient. This moderates the transmission of pulsatile pressure towards the periphery, thus protecting the microcirculatory network. The heterogeneity of stiffness between the elastic and muscular arteries causes the gradient to disappear or be inversed with aging, particularly in long-standing hypertension. Conclusions: In hypertension therefore, pulsatile pressure transmission to the microcirculation is augmented, increasing the potential risk of damage to the brain, the heart, and the kidney. Furthermore, elevated pulse pressure exacerbates end-stage renal disease, particularly in older hypertensive individuals. With increasing age, the elastin content of vessel walls declines throughout the arterial network, and arterial stiffening increases further due to the presence of rigid wall material such as collagen, but also fibronectin, proteoglycans, and vascular calcification. Certain genes, mainly related to angiotensin and/or aldosterone, affect this aging process and contribute to the extent of arterial stiffness, which can independently affect both forward and reflected pressure waves.
MeSH term(s)	Age Factors ; Arterial Pressure ; Carotid-Femoral Pulse Wave Velocity ; Disease Progression ; Essential Hypertension/complications ; Essential Hypertension/diagnosis ; Essential Hypertension/physiopathology ; Humans ; Models, Cardiovascular ; Predictive Value of Tests ; Prognosis ; Risk Factors ; Vascular Stiffness
Language	English
Publishing date	2020-02-24
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	639383-4
ISSN	1941-7225 ; 1879-1905 ; 0895-7061
ISSN (online)	1941-7225 ; 1879-1905
ISSN	0895-7061
DOI	10.1093/ajh/hpz193
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