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Article ; Online: Wide-field time-of-flight measurements of highly scattering media.

Stefanov, André / Tijkorte, Pascal / Hannink, Gijs / Roth, Lynn / Frenz, Martin

Optics letters

2023 Volume 48, Issue 24, Page(s) 6396–6399

Abstract: We present a setup that makes use of a time-resolved single-photon camera to determine the scattering parameters of media. The measurement is realized in a non-contact way, both for the illumination laser and the detection. By fitting the time-of-flight ... ...

Abstract	We present a setup that makes use of a time-resolved single-photon camera to determine the scattering parameters of media. The measurement is realized in a non-contact way, both for the illumination laser and the detection. By fitting the time-of-flight acquired distributions at different spatial positions with the diffusion equation, we retrieve the reduced scattering coefficients of a highly diffusive isotropic reference media for wavelengths in the range from 540 to 840 nm.
Language	English
Publishing date	2023-12-15
Publishing country	United States
Document type	Journal Article
ISSN	1539-4794
ISSN (online)	1539-4794
DOI	10.1364/OL.498659
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Pleiotropic Effects of Atorvastatin Result in a Downregulation of the Carboxypeptidase U System (CPU, TAFIa, CPB2) in a Mouse Model of Advanced Atherosclerosis.

Claesen, Karen / Roth, Lynn / Mertens, Joachim C / Hermans, Karlijn / Sim, Yani / Hendriks, Dirk

Pharmaceutics

2021 Volume 13, Issue 10

Abstract: Statins (hydroxymethyl-glutaryl-CoA-reductase inhibitors) lower procarboxypeptidase U (proCPU, TAFI, proCPB2). However, it is challenging to prove whether this is a lipid or non-lipid-related pleiotropic effect, since statin treatment decreases ... ...

Abstract	Statins (hydroxymethyl-glutaryl-CoA-reductase inhibitors) lower procarboxypeptidase U (proCPU, TAFI, proCPB2). However, it is challenging to prove whether this is a lipid or non-lipid-related pleiotropic effect, since statin treatment decreases cholesterol levels in humans. In apolipoprotein E-deficient mice with a heterozygous mutation in the fibrillin-1 gene (ApoE
Language	English
Publishing date	2021-10-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527217-2
ISSN	1999-4923
ISSN	1999-4923
DOI	10.3390/pharmaceutics13101731
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Article ; Online: Empagliflozin decreases ageing-associated arterial stiffening and vascular fibrosis under normoglycemic conditions.

Neutel, Cédric H G / Wesley, Callan D / Van Praet, Melissa / Civati, Celine / Roth, Lynn / De Meyer, Guido R Y / Martinet, Wim / Guns, Pieter-Jan

Vascular pharmacology

2023 Volume 152, Page(s) 107212

Abstract: Arterial stiffness is a hallmark of vascular ageing and results in increased blood flow pulsatility to the periphery, damaging end-organs such as the heart, kidneys and brain. Treating or "reversing" arterial stiffness has therefore become a central ... ...

Abstract	Arterial stiffness is a hallmark of vascular ageing and results in increased blood flow pulsatility to the periphery, damaging end-organs such as the heart, kidneys and brain. Treating or "reversing" arterial stiffness has therefore become a central target in the field of vascular ageing. SGLT2 inhibitors, initially developed in the context of type 2 diabetes mellitus, have become a cornerstone of heart failure treatment. Additionally, effects on the vasculature have been reported. Here, we demonstrate that treatment with the SGLT2 inhibitor empagliflozin (7 weeks, 15 mg/kg/day) decreased ageing-induced arterial stiffness of the aorta in old mice with normal blood glucose levels. However, no universal mechanism was identified. While empagliflozin reduced the ageing-associated increase in collagen type I in the medial layer of the abdominal infrarenal aorta and decreased medial TGF-β deposition, this was not observed in the thoracic descending aorta. Moreover, empagliflozin was not able to prevent elastin fragmentation. In conclusion, empagliflozin decreased arterial stiffness in aged mice, indicating that SGLT2 inhibition could be a valuable strategy in mitigating vascular ageing. Further research is warranted to unravel the underlying, possibly region-specific, mechanisms.
MeSH term(s)	Animals ; Mice ; Diabetes Mellitus, Type 2/drug therapy ; Arteries ; Heart ; Aging ; Aorta, Abdominal ; Sodium-Glucose Transporter 2 Inhibitors/pharmacology
Chemical Substances	empagliflozin (HDC1R2M35U) ; Sodium-Glucose Transporter 2 Inhibitors
Language	English
Publishing date	2023-08-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2082846-9
ISSN	1879-3649 ; 1537-1891 ; 1879-3649
ISSN (online)	1879-3649 ; 1537-1891
ISSN	1879-3649
DOI	10.1016/j.vph.2023.107212
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Zs.A 591: Show issues

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bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Effect of erythrophagocytosis-induced ferroptosis during angiogenesis in atherosclerotic plaques.

Puylaert, Pauline / Roth, Lynn / Van Praet, Melissa / Pintelon, Isabel / Dumitrascu, Catalina / van Nuijs, Alexander / Klejborowska, Greta / Guns, Pieter-Jan / Berghe, Tom Vanden / Augustyns, Koen / De Meyer, Guido R Y / Martinet, Wim

Angiogenesis

2023 Volume 26, Issue 4, Page(s) 505–522

Abstract: Intraplaque (IP) angiogenesis is a key feature of advanced atherosclerotic plaques. Because IP vessels are fragile and leaky, erythrocytes are released and phagocytosed by macrophages (erythrophagocytosis), which leads to high intracellular iron content, ...

Abstract	Intraplaque (IP) angiogenesis is a key feature of advanced atherosclerotic plaques. Because IP vessels are fragile and leaky, erythrocytes are released and phagocytosed by macrophages (erythrophagocytosis), which leads to high intracellular iron content, lipid peroxidation and cell death. In vitro experiments showed that erythrophagocytosis by macrophages induced non-canonical ferroptosis, an emerging type of regulated necrosis that may contribute to plaque destabilization. Erythrophagocytosis-induced ferroptosis was accompanied by increased expression of heme-oxygenase 1 and ferritin, and could be blocked by co-treatment with third generation ferroptosis inhibitor UAMC-3203. Both heme-oxygenase 1 and ferritin were also expressed in erythrocyte-rich regions of carotid plaques from ApoE
MeSH term(s)	Mice ; Animals ; Plaque, Atherosclerotic ; Ferroptosis ; Atherosclerosis ; Fibrillin-1/metabolism ; Apolipoproteins E/genetics ; Ferritins ; Oxygenases/metabolism ; Heme/metabolism
Chemical Substances	Fibrillin-1 ; Apolipoproteins E ; Ferritins (9007-73-2) ; Oxygenases (EC 1.13.-) ; Heme (42VZT0U6YR)
Language	English
Publishing date	2023-04-29
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1484717-6
ISSN	1573-7209 ; 0969-6970
ISSN (online)	1573-7209
ISSN	0969-6970
DOI	10.1007/s10456-023-09877-6
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Zs.A 5094: Show issues

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Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

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Article: Standard Immunohistochemical Assays to Assess Autophagy in Mammalian Tissue.

Martinet, Wim / Roth, Lynn / De Meyer, Guido R Y

Cells

2017 Volume 6, Issue 3

Abstract: Autophagy is a highly conserved lysosomal degradation pathway with major impact on diverse human pathologies. Despite the development of different methodologies to detect autophagy both in vitro and in vivo, monitoring autophagy in tissue via ... ...

Abstract	Autophagy is a highly conserved lysosomal degradation pathway with major impact on diverse human pathologies. Despite the development of different methodologies to detect autophagy both in vitro and in vivo, monitoring autophagy in tissue via immunohistochemical techniques is hampered due to the lack of biomarkers. Immunohistochemical detection of a punctate pattern of ATG8/MAP1LC3 proteins is currently the most frequently used approach to detect autophagy in situ, but it depends on a highly sensitive detection method and is prone to misinterpretation. Moreover, reliable MAP1LC3 immunohistochemical staining requires correct tissue processing and high-quality, isoform-specific antibodies. Immunohistochemical analysis of other autophagy-related protein targets such as SQSTM1, ubiquitin, ATG5 or lysosomal proteins is not recommended as marker for autophagic activity in tissue for multiple reasons including aspecific labeling of cellular structures and a lack of differential protein expression during autophagy initiation. To better understand the role of autophagy in human disease, novel biomarkers for visualization of the autophagic process with standard histology techniques are urgently needed.
Language	English
Publishing date	2017-06-30
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661518-6
ISSN	2073-4409
ISSN	2073-4409
DOI	10.3390/cells6030017
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Article ; Online: Acetylsalicylic Acid Reduces Passive Aortic Wall Stiffness and Cardiovascular Remodelling in a Mouse Model of Advanced Atherosclerosis.

Roth, Lynn / Rombouts, Miche / Schrijvers, Dorien M / Emini Veseli, Besa / Martinet, Wim / De Meyer, Guido R Y

International journal of molecular sciences

2021 Volume 23, Issue 1

Abstract: Acetylsalicylic acid (ASA) is widely used in secondary prevention of cardiovascular (CV) disease, mainly because of its antithrombotic effects. Here, we investigated whether ASA can prevent the progression of vessel wall remodelling, atherosclerosis, and ...

Abstract	Acetylsalicylic acid (ASA) is widely used in secondary prevention of cardiovascular (CV) disease, mainly because of its antithrombotic effects. Here, we investigated whether ASA can prevent the progression of vessel wall remodelling, atherosclerosis, and CV complications in apolipoprotein E deficient (
MeSH term(s)	Animals ; Aorta/drug effects ; Aorta/pathology ; Aorta/physiopathology ; Apolipoproteins E/deficiency ; Apolipoproteins E/metabolism ; Aspirin/pharmacology ; Atherosclerosis/pathology ; Atherosclerosis/physiopathology ; Blood Pressure/drug effects ; Disease Models, Animal ; Disease Progression ; Female ; Fibrillin-1/metabolism ; Kaplan-Meier Estimate ; Lymphocytes/drug effects ; Lymphocytes/metabolism ; Mice ; Myocardial Infarction/physiopathology ; Neutrophils/drug effects ; Neutrophils/metabolism ; Vascular Remodeling/drug effects ; Vascular Stiffness/drug effects
Chemical Substances	Apolipoproteins E ; Fibrillin-1 ; Aspirin (R16CO5Y76E)
Language	English
Publishing date	2021-12-30
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/ijms23010404
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Article ; Online: Doxorubicin-induced cardiovascular toxicity: a longitudinal evaluation of functional and molecular markers.

Bosman, Matthias / Krüger, Dustin / Van Assche, Charles / Boen, Hanne / Neutel, Cédric / Favere, Kasper / Franssen, Constantijn / Martinet, Wim / Roth, Lynn / De Meyer, Guido R Y / Cillero-Pastor, Berta / Delrue, Leen / Heggermont, Ward / Van Craenenbroeck, Emeline M / Guns, Pieter-Jan

Cardiovascular research

2023 Volume 119, Issue 15, Page(s) 2579–2590

Abstract: Aims: Apart from cardiotoxicity, the chemotherapeutic doxorubicin (DOX) induces vascular toxicity, represented by arterial stiffness and endothelial dysfunction. Both parameters are of interest for cardiovascular risk stratification as they are ... ...

Abstract	Aims: Apart from cardiotoxicity, the chemotherapeutic doxorubicin (DOX) induces vascular toxicity, represented by arterial stiffness and endothelial dysfunction. Both parameters are of interest for cardiovascular risk stratification as they are independent predictors of future cardiovascular events in the general population. However, the time course of DOX-induced cardiovascular toxicity remains unclear. Moreover, current biomarkers for cardiovascular toxicity prove insufficient. Here, we longitudinally evaluated functional and molecular markers of DOX-induced cardiovascular toxicity in a murine model. Molecular markers were further validated in patient plasma. Methods and results: DOX (4 mg/kg) or saline (vehicle) was administered intra-peritoneally to young, male mice weekly for 6 weeks. In vivo cardiovascular function and ex vivo arterial stiffness and vascular reactivity were evaluated at baseline, during DOX therapy (Weeks 2 and 4) and after therapy cessation (Weeks 6, 9, and 15). Left ventricular ejection fraction (LVEF) declined from Week 4 in the DOX group. DOX increased arterial stiffness in vivo and ex vivo at Week 2, which reverted thereafter. Importantly, DOX-induced arterial stiffness preceded reduced LVEF. Further, DOX impaired endothelium-dependent vasodilation at Weeks 2 and 6, which recovered at Weeks 9 and 15. Conversely, contraction with phenylephrine was consistently higher in the DOX-treated group. Furthermore, proteomic analysis on aortic tissue identified increased thrombospondin-1 (THBS1) and alpha-1-antichymotrypsin (SERPINA3) at Weeks 2 and 6. Up-regulated THBS1 and SERPINA3 persisted during follow-up. Finally, THBS1 and SERPINA3 were quantified in plasma of patients. Cancer survivors with anthracycline-induced cardiotoxicity (AICT; LVEF < 50%) showed elevated THBS1 and SERPINA3 levels compared with age-matched control patients (LVEF ≥ 60%). Conclusions: DOX increased arterial stiffness and impaired endothelial function, which both preceded reduced LVEF. Vascular dysfunction restored after DOX therapy cessation, whereas cardiac dysfunction persisted. Further, we identified SERPINA3 and THBS1 as promising biomarkers of DOX-induced cardiovascular toxicity, which were confirmed in AICT patients.
MeSH term(s)	Humans ; Male ; Mice ; Animals ; Cardiotoxicity/drug therapy ; Stroke Volume ; Proteomics ; Ventricular Function, Left ; Doxorubicin/toxicity ; Biomarkers
Chemical Substances	Doxorubicin (80168379AG) ; Biomarkers
Language	English
Publishing date	2023-08-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvad136
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Zs.A 565: Show issues

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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)

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Article: Gasdermin D Deficiency Limits the Transition of Atherosclerotic Plaques to an Inflammatory Phenotype in

Puylaert, Pauline / Van Praet, Melissa / Vaes, Frederik / Neutel, Cédric H G / Roth, Lynn / Guns, Pieter-Jan / De Meyer, Guido R Y / Martinet, Wim

Biomedicines

2022 Volume 10, Issue 5

Abstract: Gasdermin D (GSDMD) is the key executor of pyroptotic cell death. Recent studies suggest that GSDMD-mediated pyroptosis is involved in atherosclerotic plaque destabilization. We report that cleaved GSDMD is expressed in macrophage- and smooth muscle cell- ...

Abstract	Gasdermin D (GSDMD) is the key executor of pyroptotic cell death. Recent studies suggest that GSDMD-mediated pyroptosis is involved in atherosclerotic plaque destabilization. We report that cleaved GSDMD is expressed in macrophage- and smooth muscle cell-rich areas of human plaques. To determine the effects of GSDMD deficiency on atherogenesis,
Language	English
Publishing date	2022-05-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines10051171
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Article: Defective Autophagy in Vascular Smooth Muscle Cells Alters Vascular Reactivity of the Mouse Femoral Artery.

De Munck, Dorien G / De Moudt, Sofie / Roth, Lynn / De Meyer, Guido R Y / Martinet, Wim / Fransen, Paul

Frontiers in physiology

2020 Volume 11, Page(s) 548943

Abstract: Autophagy is an important cellular survival process that enables degradation and recycling of defective organelles and proteins to maintain cellular homeostasis. Hence, defective autophagy plays a role in many age-associated diseases, such as ... ...

Abstract	Autophagy is an important cellular survival process that enables degradation and recycling of defective organelles and proteins to maintain cellular homeostasis. Hence, defective autophagy plays a role in many age-associated diseases, such as atherosclerosis, arterial stiffening and hypertension. Recently, we showed in mice that autophagy in vascular smooth muscle cells (VSMCs) of large elastic arteries such as the aorta is important for Ca
Language	English
Publishing date	2020-09-23
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2020.548943
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Article ; Online: Defective Autophagy in Atherosclerosis: To Die or to Senesce?

Grootaert, Mandy O J / Roth, Lynn / Schrijvers, Dorien M / De Meyer, Guido R Y / Martinet, Wim

Oxidative medicine and cellular longevity

2018 Volume 2018, Page(s) 7687083

Abstract: Autophagy is a subcellular process that plays an important role in the degradation of proteins and damaged organelles such as mitochondria (a process termed "mitophagy") via lysosomes. It is crucial for regulating protein and mitochondrial quality ... ...

Abstract	Autophagy is a subcellular process that plays an important role in the degradation of proteins and damaged organelles such as mitochondria (a process termed "mitophagy") via lysosomes. It is crucial for regulating protein and mitochondrial quality control and maintaining cellular homeostasis, whereas dysregulation of autophagy has been implicated in a wide range of diseases including atherosclerosis. Recent evidence has shown that the autophagic process becomes dysfunctional during the progression of atherosclerosis, regardless of whether there are many autophagy-stimulating factors (e.g., reactive oxygen species, oxidized lipids, and cytokines) present within the atherosclerotic plaque. This review highlights the recent insights into the causes and consequences of defective autophagy in atherosclerosis, with a special focus on the role of autophagy and mitophagy in plaque macrophages, vascular smooth muscle cells (VSMCs), and endothelial cells (ECs). It has been shown that defective autophagy can promote apoptosis in macrophages but that it accelerates premature senescence in VSMCs. In the ECs, defective autophagy promotes both apoptosis and senescence. We will discuss the discrepancy between these three cell types in their response to autophagy deficiency and underline the cell type-dependent role of autophagy, which may have important implications for the efficacy of autophagy-targeted treatments for atherosclerosis.
MeSH term(s)	Animals ; Apoptosis/physiology ; Atherosclerosis/metabolism ; Atherosclerosis/physiopathology ; Autophagy/physiology ; Cellular Senescence/physiology ; Humans ; Mitochondrial Degradation/physiology
Language	English
Publishing date	2018-02-26
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1942-0994
ISSN (online)	1942-0994
DOI	10.1155/2018/7687083
Database	MEDical Literature Analysis and Retrieval System OnLINE

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