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  1. Article ; Online: Programmed death of macrophages in atherosclerosis: mechanisms and therapeutic targets.

    De Meyer, Guido R Y / Zurek, Michelle / Puylaert, Pauline / Martinet, Wim

    Nature reviews. Cardiology

    2024  Volume 21, Issue 5, Page(s) 312–325

    Abstract: Atherosclerosis is a progressive inflammatory disorder of the arterial vessel wall characterized by substantial infiltration of macrophages, which exert both favourable and detrimental functions. Early in atherogenesis, macrophages can clear cytotoxic ... ...

    Abstract Atherosclerosis is a progressive inflammatory disorder of the arterial vessel wall characterized by substantial infiltration of macrophages, which exert both favourable and detrimental functions. Early in atherogenesis, macrophages can clear cytotoxic lipoproteins and dead cells, preventing cytotoxicity. Efferocytosis - the efficient clearance of dead cells by macrophages - is crucial for preventing secondary necrosis and stimulating the release of anti-inflammatory cytokines. In addition, macrophages can promote tissue repair and proliferation of vascular smooth muscle cells, thereby increasing plaque stability. However, advanced atherosclerotic plaques contain large numbers of pro-inflammatory macrophages that secrete matrix-degrading enzymes, induce death in surrounding cells and contribute to plaque destabilization and rupture. Importantly, macrophages in the plaque can undergo apoptosis and several forms of regulated necrosis, including necroptosis, pyroptosis and ferroptosis. Regulated necrosis has an important role in the formation and expansion of the necrotic core during plaque progression, and several triggers for necrosis are present within atherosclerotic plaques. This Review focuses on the various forms of programmed macrophage death in atherosclerosis and the pharmacological interventions that target them as a potential means of stabilizing vulnerable plaques and improving the efficacy of currently available anti-atherosclerotic therapies.
    MeSH term(s) Humans ; Plaque, Atherosclerotic ; Atherosclerosis/drug therapy ; Macrophages/physiology ; Apoptosis ; Necrosis
    Language English
    Publishing date 2024-01-02
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2490375-9
    ISSN 1759-5010 ; 1759-5002
    ISSN (online) 1759-5010
    ISSN 1759-5002
    DOI 10.1038/s41569-023-00957-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Plasma levels of autophagy regulator Rubicon are inversely associated with acute coronary syndrome.

    Grazide, Marie-Hélène / Ruidavets, Jean-Bernard / Martinet, Wim / Elbaz, Meyer / Vindis, Cécile

    Frontiers in cardiovascular medicine

    2024  Volume 10, Page(s) 1279899

    Abstract: Background: The discovery of novel biomarkers that improve current cardiovascular risk prediction models of acute coronary syndrome (ACS) is needed for the identification of very high-risk patients and therapeutic decision-making. Autophagy is a highly ... ...

    Abstract Background: The discovery of novel biomarkers that improve current cardiovascular risk prediction models of acute coronary syndrome (ACS) is needed for the identification of very high-risk patients and therapeutic decision-making. Autophagy is a highly conserved catabolic mechanism for intracellular degradation of cellular components through lysosomes. The autophagy process helps maintain cardiac homeostasis and dysregulated autophagy has been described in cardiovascular conditions. Rubicon (Run domain Beclin-1-interacting and cysteine-rich domain-containing protein) is a key regulator of autophagy with a potential role in cardiac stress.
    Objectives: The aims of the present study were to assess whether changes in circulating Rubicon levels are associated with ACS and to evaluate the added value of Rubicon to a clinical predictive risk model.
    Methods and results: The study population included ACS patients (
    Conclusions: Plasma levels of the autophagy regulator Rubicon are associated with ACS and provide added value to classical risk markers for ACS.
    Language English
    Publishing date 2024-01-05
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2781496-8
    ISSN 2297-055X
    ISSN 2297-055X
    DOI 10.3389/fcvm.2023.1279899
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Association of circulating autophagy proteins ATG5 and Beclin 1 with acute myocardial infarction in a case-control study.

    Grazide, Marie-Hélène / Ruidavets, Jean-Bernard / Martinet, Wim / Elbaz, Meyer / Vindis, Cécile

    Cardiology

    2024  

    Abstract: Introduction: Acute myocardial infarction (AMI) is a main contributor of sudden cardiac death worldwide. The discovery of new biomarkers that can improve AMI risk prediction meets a major clinical need for the identification of high-risk patients and ... ...

    Abstract Introduction: Acute myocardial infarction (AMI) is a main contributor of sudden cardiac death worldwide. The discovery of new biomarkers that can improve AMI risk prediction meets a major clinical need for the identification of high-risk patients and the tailoring of medical treatment. Previously, we reported that autophagy a highly conserved catabolic mechanism for intracellular degradation of cellular components, is involved in atherosclerotic plaque phenotype and cardiac pathological remodeling. The crucial role of autophagy in the normal and diseased heart has been well described, and its activation functions as a pro-survival process in response to myocardial ischemia. However, autophagy is dysregulated in ischemia/reperfusion injury thus promoting necrotic or apoptotic cardiac cell death. Very few studies have focused on the plasma levels of autophagy markers in cardiovascular disease patients, even though they could be companion biomarkers of AMI injury. The aims of the present study were to evaluate: 1) whether variations in plasma levels of two key autophagy regulators ATG5 (Autophagy-related gene 5) and Beclin 1 (the mammalian yeast ortholog Atg6/Vps30) are associated with AMI and 2) their potential for predicting AMI risk.
    Methods: The case-control study population included AMI patients (n = 100) and control subjects (n = 99) at high cardiovascular risk but without known coronary disease. Plasma levels of ATG5 and Beclin 1 were measured in the whole population study by enzyme-linked immunosorbent assay.
    Results: Multivariate analyses adjusted on common cardiovascular factors and medical treatments, and receiver operating characteristic (ROC) curves demonstrated that: ATG5 and Beclin 1 levels were inversely associated with AMI and provided original biomarkers for AMI risk prediction.
    Conclusion: Plasma levels of autophagy regulators ATG5 and Beclin 1 represent relevant candidate biomarkers associated with AMI.
    Language English
    Publishing date 2024-03-02
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 80092-2
    ISSN 1421-9751 ; 0008-6312
    ISSN (online) 1421-9751
    ISSN 0008-6312
    DOI 10.1159/000537816
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  4. Article: The effect of cyclic stretch on aortic viscoelasticity and the putative role of smooth muscle focal adhesion.

    Neutel, Cédric H G / Wesley, Callan D / De Meyer, Guido R Y / Martinet, Wim / Guns, Pieter-Jan

    Frontiers in physiology

    2023  Volume 14, Page(s) 1218924

    Abstract: Due to its viscoelastic properties, the aorta aids in dampening blood pressure pulsatility. At the level of resistance-arteries, the pulsatile flow will be transformed into a continuous flow to allow for optimal perfusion of end organs such as the ... ...

    Abstract Due to its viscoelastic properties, the aorta aids in dampening blood pressure pulsatility. At the level of resistance-arteries, the pulsatile flow will be transformed into a continuous flow to allow for optimal perfusion of end organs such as the kidneys and the brain. In this study, we investigated the
    Language English
    Publishing date 2023-08-11
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2023.1218924
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  5. Article: Basal Vascular Smooth Muscle Cell Tone in eNOS Knockout Mice Can Be Reversed by Cyclic Stretch and Is Independent of Age.

    De Moudt, Sofie / Hendrickx, Jhana O / De Meyer, Guido R Y / Martinet, Wim / Fransen, Paul

    Frontiers in physiology

    2022  Volume 13, Page(s) 882527

    Abstract: Introduction and Aims: ...

    Abstract Introduction and Aims:
    Language English
    Publishing date 2022-04-28
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2022.882527
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  6. Article ; Online: Regulated Necrosis in Atherosclerosis.

    Puylaert, Pauline / Zurek, Michelle / Rayner, Katey J / De Meyer, Guido R Y / Martinet, Wim

    Arteriosclerosis, thrombosis, and vascular biology

    2022  Volume 42, Issue 11, Page(s) 1283–1306

    Abstract: During atherosclerosis, lipid-rich plaques are formed in large- and medium-sized arteries, which can reduce blood flow to tissues. This situation becomes particularly precarious when a plaque develops an unstable phenotype and becomes prone to rupture. ... ...

    Abstract During atherosclerosis, lipid-rich plaques are formed in large- and medium-sized arteries, which can reduce blood flow to tissues. This situation becomes particularly precarious when a plaque develops an unstable phenotype and becomes prone to rupture. Despite advances in identifying and treating vulnerable plaques, the mortality rate and disability caused by such lesions remains the number one health threat in developed countries. Vulnerable, unstable plaques are characterized by a large necrotic core, implying a prominent role for necrotic cell death in atherosclerosis and plaque destabilization. Necrosis can occur accidentally or can be induced by tightly regulated pathways. Over the past decades, different forms of regulated necrosis, including necroptosis, ferroptosis, pyroptosis, and secondary necrosis, have been identified, and these may play an important role during atherogenesis. In this review, we describe several forms of necrosis that may occur in atherosclerosis and how pharmacological modulation of these pathways can stabilize vulnerable plaques. Moreover, some challenges of targeting necrosis in atherosclerosis such as the presence of multiple death-inducing stimuli in plaques and extensive cross-talk between necrosis pathways are discussed. A better understanding of the role of (regulated) necrosis in atherosclerosis and the mechanisms contributing to plaque destabilization may open doors to novel pharmacological strategies and will enable clinicians to tackle the residual cardiovascular risk that remains in many atherosclerosis patients.
    MeSH term(s) Humans ; Atherosclerosis/pathology ; Necrosis ; Plaque, Atherosclerotic/pathology ; Apoptosis ; Lipids
    Chemical Substances Lipids
    Language English
    Publishing date 2022-09-22
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1221433-4
    ISSN 1524-4636 ; 1079-5642
    ISSN (online) 1524-4636
    ISSN 1079-5642
    DOI 10.1161/ATVBAHA.122.318177
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1705: Show issues Location:
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  7. Article ; Online: Disparate biomechanical properties of the aorta in non-aneurysmal and aneurysmal mice treated with angiotensin II.

    De Moudt, Sofie / Hendrickx, Jhana O / De Meyer, Guido R Y / Martinet, Wim / Fransen, Paul

    Physiological reports

    2022  Volume 10, Issue 18, Page(s) e15410

    Abstract: In vivo angiotensin II (AngII)-treatment is a widely used experimental model to induce cardiovascular disease and results in a high likelihood of abdominal aorta aneurysm (AAA) formation. This involves progressive and irreversible focal dilation of the ... ...

    Abstract In vivo angiotensin II (AngII)-treatment is a widely used experimental model to induce cardiovascular disease and results in a high likelihood of abdominal aorta aneurysm (AAA) formation. This involves progressive and irreversible focal dilation of the abdominal aorta and induces adverse aortic connective tissue remodeling contributing to aortic wall stiffening through inflammation, elastin degradation, and collagen restructuring. Hence, the present study aimed to investigate how AAA formation in AngII-treated mice affects aortic function and biomechanics. To this end, C57Bl/6J mice were treated with AngII (1000 ng/[kg.min]) or PBS infusion for 28 days. Peripheral blood pressure, echocardiography, and aortic pulse wave velocity were measured in vivo. Thoracic aorta rings were studied ex vivo in organ chambers, while aortic vascular smooth muscle cell (VSMC) phenotype was investigated histologically. We confirmed peripheral hypertension, cardiac hypertrophy, aortic stiffening, and increased VSMC proliferation and migration after AngII-treatment. Abdominal aorta aneurysm formation was observed in 8/13 AngII-treated mice. Ex vivo thoracic aortic rings of both aneurysmal and non-aneurysmal AngII-treated mice showed high isobaric aortic stiffness, endothelial dysfunction, heightened α
    MeSH term(s) Adrenergic Agents/metabolism ; Angiotensin II/metabolism ; Animals ; Aorta, Abdominal/metabolism ; Aortic Aneurysm, Abdominal/metabolism ; Collagen/metabolism ; Elastin/metabolism ; Mice ; Mice, Inbred C57BL ; Pulse Wave Analysis
    Chemical Substances Adrenergic Agents ; Angiotensin II (11128-99-7) ; Collagen (9007-34-5) ; Elastin (9007-58-3)
    Language English
    Publishing date 2022-09-14
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2724325-4
    ISSN 2051-817X ; 2051-817X
    ISSN (online) 2051-817X
    ISSN 2051-817X
    DOI 10.14814/phy2.15410
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  8. Article ; Online: Autophagy as an emerging therapeutic target for age-related vascular pathologies.

    De Munck, Dorien G / De Meyer, Guido Ry / Martinet, Wim

    Expert opinion on therapeutic targets

    2020  Volume 24, Issue 2, Page(s) 131–145

    Abstract: ... ...

    Abstract Introduction
    MeSH term(s) Aging ; Animals ; Autophagy/drug effects ; Endothelial Cells/metabolism ; Humans ; Molecular Targeted Therapy ; Myocytes, Smooth Muscle/metabolism ; Vascular Diseases/drug therapy ; Vascular Diseases/physiopathology
    Language English
    Publishing date 2020-02-03
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2055208-7
    ISSN 1744-7631 ; 1472-8222
    ISSN (online) 1744-7631
    ISSN 1472-8222
    DOI 10.1080/14728222.2020.1723079
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    Zs.A 5244: Show issues Location:
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  9. Article: Inflammation, Nitro-Oxidative Stress, Impaired Autophagy, and Insulin Resistance as a Mechanistic Convergence Between Arterial Stiffness and Alzheimer's Disease.

    Hendrickx, Jhana O / Martinet, Wim / Van Dam, Debby / De Meyer, Guido R Y

    Frontiers in molecular biosciences

    2021  Volume 8, Page(s) 651215

    Abstract: The average age of the world's elderly population is steadily increasing. This unprecedented rise in the aged world population will increase the prevalence of age-related disorders such as cardiovascular disease (CVD) and neurodegeneration. In recent ... ...

    Abstract The average age of the world's elderly population is steadily increasing. This unprecedented rise in the aged world population will increase the prevalence of age-related disorders such as cardiovascular disease (CVD) and neurodegeneration. In recent years, there has been an increased interest in the potential interplay between CVDs and neurodegenerative syndromes, as several vascular risk factors have been associated with Alzheimer's disease (AD). Along these lines, arterial stiffness is an independent risk factor for both CVD and AD. In this review, we discuss several inflammaging-related disease mechanisms including acute tissue-specific inflammation, nitro-oxidative stress, impaired autophagy, and insulin resistance which may contribute to the proposed synergism between arterial stiffness and AD.
    Language English
    Publishing date 2021-03-29
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2814330-9
    ISSN 2296-889X
    ISSN 2296-889X
    DOI 10.3389/fmolb.2021.651215
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  10. Article ; Online: The PFKFB3 Inhibitor AZ67 Inhibits Angiogenesis Independently of Glycolysis Inhibition.

    Emini Veseli, Besa / Van Wielendaele, Pieter / Delibegovic, Mirela / Martinet, Wim / De Meyer, Guido R Y

    International journal of molecular sciences

    2021  Volume 22, Issue 11

    Abstract: Angiogenesis is the process of new blood vessel formation. In this complex orchestrated growth, many factors are included. Lately, focus has shifted to endothelial cell metabolism, particularly to the PFKFB3 protein, a key regulatory enzyme of the ... ...

    Abstract Angiogenesis is the process of new blood vessel formation. In this complex orchestrated growth, many factors are included. Lately, focus has shifted to endothelial cell metabolism, particularly to the PFKFB3 protein, a key regulatory enzyme of the glycolytic pathway. A variety of inhibitors of this important target have been studied, and a plethora of biological effects related to the process of angiogenesis have been reported. However, recent studies have disputed their mechanism of action, questioning whether all the effects are indeed due to PFKFB3 inhibition. Remarkably, the most well-studied inhibitor, 3PO, does not bind to PFKFB3, raising questions about this target. In our study, we aimed to elucidate the effects of PFKFB3 inhibition in angiogenesis by using the small molecule AZ67. We used isothermal titration calorimetry and confirmed binding to PFKFB3. In vitro, AZ67 did not decrease lactate production in endothelial cells (ECs), nor ATP levels, but exhibited good inhibitory efficacy in the tube-formation assay. Surprisingly, this was independent of EC migratory and proliferative abilities, as this was not diminished upon treatment. Strikingly however, even the lowest dose of AZ67 demonstrated significant inhibition of angiogenesis in vivo. To our knowledge, this is the first study to demonstrate that the process of angiogenesis can be disrupted by targeting PFKFB3 independently of glycolysis inhibition.
    MeSH term(s) Animals ; Cell Line ; Cell Proliferation/drug effects ; Endothelial Cells ; Enzyme Inhibitors/metabolism ; Enzyme Inhibitors/pharmacology ; Glycolysis/drug effects ; Humans ; Mice ; Mice, Inbred C57BL ; Neovascularization, Physiologic/drug effects ; Phosphofructokinase-2/antagonists & inhibitors ; Phosphofructokinase-2/metabolism ; Protein Binding
    Chemical Substances Enzyme Inhibitors ; PFKFB3 protein, human (EC 2.7.1.105) ; Phosphofructokinase-2 (EC 2.7.1.105)
    Language English
    Publishing date 2021-05-31
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms22115970
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