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Article ; Online: The Prognostic, Diagnostic, and Therapeutic Potential of TRAIL Signalling in Cardiovascular Diseases.

Kelland, Elaina / Patil, Manisha S / Patel, Sanjay / Cartland, Siân P / Kavurma, Mary M

International journal of molecular sciences

2023 Volume 24, Issue 7

Abstract: TNF-related apoptosis-inducing ligand (TRAIL) was originally discovered, almost 20 years ago, for its ability to kill cancer cells. More recent evidence has described pleiotropic functions, particularly in the cardiovascular system. There is potential ... ...

Abstract	TNF-related apoptosis-inducing ligand (TRAIL) was originally discovered, almost 20 years ago, for its ability to kill cancer cells. More recent evidence has described pleiotropic functions, particularly in the cardiovascular system. There is potential for TRAIL concentrations in the circulation to act as prognostic and/or diagnostic factors for cardiovascular diseases (CVD). Pre-clinical studies also describe the therapeutic capacity for TRAIL signals, particularly in the context of atherosclerotic disease and diseases of the myocardium. Because diabetes mellitus significantly contributes to the progression and pathogenesis of CVDs, in this review we highlight recent evidence for the prognostic, diagnostic, and therapeutic potential of TRAIL signals in CVDs, and where relevant, the impact of diabetes mellitus. A greater understanding of how TRAIL signals regulate cardiovascular protection and pathology may offer new diagnostic and therapeutic avenues for patients suffering from CVDs.
MeSH term(s)	Humans ; Cardiovascular Diseases/diagnosis ; Cardiovascular Diseases/therapy ; Cardiovascular Diseases/complications ; TNF-Related Apoptosis-Inducing Ligand/therapeutic use ; Prognosis ; Atherosclerosis/pathology ; Diabetes Mellitus ; Apoptosis
Chemical Substances	TNF-Related Apoptosis-Inducing Ligand
Language	English
Publishing date	2023-04-04
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24076725
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: TRAIL signals, extracellular matrix and vessel remodelling.

Patil, Manisha S / Cartland, Siân P / Kavurma, Mary M

Vascular biology (Bristol, England)

2020 Volume 2, Issue 1, Page(s) R73–R84

Abstract: The extracellular matrix (ECM) is an essential part of the vasculature, not only providing structural support to the blood vessel wall, but also in its ability to interact with cells to regulate cell phenotype and function including proliferation, ... ...

Abstract	The extracellular matrix (ECM) is an essential part of the vasculature, not only providing structural support to the blood vessel wall, but also in its ability to interact with cells to regulate cell phenotype and function including proliferation, migration, differentiation and death - processes important in vascular remodelling. Increasing evidence implicates TNF-related apoptosis-inducing ligand (TRAIL) signalling in the modulation of vascular cell function and remodelling under normal and pathological conditions such as in atherosclerosis. TRAIL can also stimulate synthesis of multiple ECM components within blood vessels. This review explores the relationship between TRAIL signals, the ECM, and its implications in vessel remodelling in cardiovascular disease.
Language	English
Publishing date	2020-06-15
Publishing country	England
Document type	Journal Article ; Review
ISSN	2516-5658
ISSN (online)	2516-5658
DOI	10.1530/VB-20-0005
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Article ; Online: The Prognostic, Diagnostic, and Therapeutic Potential of TRAIL Signalling in Cardiovascular Diseases

Elaina Kelland / Manisha S. Patil / Sanjay Patel / Siân P. Cartland / Mary M. Kavurma

International Journal of Molecular Sciences, Vol 24, Iss 6725, p

2023 Volume 6725

Abstract	TNF-related apoptosis-inducing ligand (TRAIL) was originally discovered, almost 20 years ago, for its ability to kill cancer cells. More recent evidence has described pleiotropic functions, particularly in the cardiovascular system. There is potential for TRAIL concentrations in the circulation to act as prognostic and/or diagnostic factors for cardiovascular diseases (CVD). Pre-clinical studies also describe the therapeutic capacity for TRAIL signals, particularly in the context of atherosclerotic disease and diseases of the myocardium. Because diabetes mellitus significantly contributes to the progression and pathogenesis of CVDs, in this review we highlight recent evidence for the prognostic, diagnostic, and therapeutic potential of TRAIL signals in CVDs, and where relevant, the impact of diabetes mellitus. A greater understanding of how TRAIL signals regulate cardiovascular protection and pathology may offer new diagnostic and therapeutic avenues for patients suffering from CVDs.
Keywords	TRAIL ; diagnostic and therapeutic potential ; atherosclerosis ; heart failure ; diabetes ; clinical and pre-clinical studies ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2023-04-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Broad-spectrum chemokine inhibition blocks inflammation-induced angiogenesis, but preserves ischemia-driven angiogenesis.

Ravindran, Dhanya / Cartland, Siân P / Bursill, Christina A / Kavurma, Mary M

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2019 Volume 33, Issue 12, Page(s) 13423–13434

Abstract: M3 is a broad-spectrum chemokine-binding protein that inactivates inflammatory chemokines, including CCL2, CCL5, and ... ...

Abstract	M3 is a broad-spectrum chemokine-binding protein that inactivates inflammatory chemokines, including CCL2, CCL5, and CX
MeSH term(s)	Adenoviridae/genetics ; Animals ; Cell Movement ; Cell Proliferation ; Chemokines/metabolism ; Hindlimb/physiology ; Hypoxia/complications ; Inflammation/complications ; Ischemia/complications ; Kruppel-Like Factor 4 ; Macrophages/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout, ApoE ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Neovascularization, Pathologic/etiology ; Neovascularization, Pathologic/pathology ; Neovascularization, Pathologic/prevention & control ; Regional Blood Flow ; Signal Transduction ; Viral Proteins/antagonists & inhibitors ; Viral Proteins/genetics
Chemical Substances	Chemokines ; KLF4 protein, human ; Klf4 protein, mouse ; Kruppel-Like Factor 4 ; M3 protein, Murine gammaherpesvirus ; Viral Proteins
Language	English
Publishing date	2019-10-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.201900232RR
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Zs.A 2266: 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 296: Show issues

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Article ; Online: The multiple roles of chemokines in the mechanisms of stent biocompatibility.

Ravindran, Dhanya / Karimi Galougahi, Keyvan / Tan, Joanne T M / Kavurma, Mary M / Bursill, Christina A

Cardiovascular research

2020 Volume 117, Issue 11, Page(s) 2299–2308

Abstract: While the advent of drug-eluting stents has been clinically effective in substantially reducing the rates of major stent-related adverse events compared with bare metal stents, vascular biological problems such as neointimal hyperplasia, delayed re- ... ...

Abstract	While the advent of drug-eluting stents has been clinically effective in substantially reducing the rates of major stent-related adverse events compared with bare metal stents, vascular biological problems such as neointimal hyperplasia, delayed re-endothelialization, late stent thrombosis are not eliminated and, increasingly, neoatherosclerosis is the underlying mechanism for very late stent failure. Further understanding regarding the mechanisms underlying the biological responses to stent deployment is therefore required so that new and improved therapies can be developed. This review will discuss the accumulating evidence that the chemokines, small inflammatory proteins, play a role in each key biological process of stent biocompatibility. It will address the chemokine system in its specialized roles in regulating the multiple facets of vascular biocompatibility including neointimal hyperplasia, endothelial progenitor cell (EPC) mobilization and re-endothelialization after vascular injury, platelet activation and thrombosis, as well as neoatherosclerosis. The evidence in this review suggests that chemokine-targeting strategies may be effective in controlling the pathobiological processes that lead to stent failure. Preclinical studies provide evidence that inhibition of specific chemokines and/or broad-spectrum inhibition of the CC-chemokine class prevents neointimal hyperplasia, reduces thrombosis and suppresses the development of neoatherosclerosis. In contrast, however, to these apparent deleterious effects of chemokines on stent biocompatibility, the CXC chemokine, CXCL12, is essential for the mobilization and recruitment of EPCs that make important contributions to re-endothelialization post-stent deployment. This suggests that future chemokine inhibition strategies would need to be correctly targeted so that all key stent biocompatibility areas could be addressed, without compromising important adaptive biological responses.
MeSH term(s)	Animals ; Biocompatible Materials ; Chemokines/immunology ; Chemokines/metabolism ; Coronary Artery Disease/immunology ; Coronary Artery Disease/metabolism ; Coronary Artery Disease/pathology ; Coronary Artery Disease/therapy ; Coronary Restenosis/immunology ; Coronary Restenosis/metabolism ; Coronary Restenosis/pathology ; Coronary Thrombosis/immunology ; Coronary Thrombosis/metabolism ; Coronary Thrombosis/pathology ; Coronary Vessels/immunology ; Coronary Vessels/metabolism ; Coronary Vessels/pathology ; Drug-Eluting Stents ; Humans ; Hyperplasia ; Neointima ; Percutaneous Coronary Intervention/adverse effects ; Percutaneous Coronary Intervention/instrumentation ; Prosthesis Design ; Signal Transduction ; Stents ; Treatment Outcome
Chemical Substances	Biocompatible Materials ; Chemokines
Language	English
Publishing date	2020-02-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvaa072
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Zs.A 565: Show issues

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Article ; Online: Sex, Endothelial Cell Functions, and Peripheral Artery Disease.

Cartland, Siân P / Stanley, Christopher P / Bursill, Christina / Passam, Freda / Figtree, Gemma A / Patel, Sanjay / Loa, Jacky / Golledge, Jonathan / Robinson, David A / Aitken, Sarah J / Kavurma, Mary M

International journal of molecular sciences

2023 Volume 24, Issue 24

Abstract: Peripheral artery disease (PAD) is caused by blocked arteries due to atherosclerosis and/or thrombosis which reduce blood flow to the lower limbs. It results in major morbidity, including ischemic limb, claudication, and amputation, with patients also ... ...

Abstract	Peripheral artery disease (PAD) is caused by blocked arteries due to atherosclerosis and/or thrombosis which reduce blood flow to the lower limbs. It results in major morbidity, including ischemic limb, claudication, and amputation, with patients also suffering a heightened risk of heart attack, stroke, and death. Recent studies suggest women have a higher prevalence of PAD than men, and with worse outcomes after intervention. In addition to a potential unconscious bias faced by women with PAD in the health system, with underdiagnosis, and lower rates of guideline-based therapy, fundamental biological differences between men and women may be important. In this review, we highlight sexual dimorphisms in endothelial cell functions and how they may impact PAD pathophysiology in women. Understanding sex-specific mechanisms in PAD is essential for the development of new therapies and personalized care for patients with PAD.
MeSH term(s)	Male ; Humans ; Female ; Peripheral Arterial Disease/therapy ; Atherosclerosis ; Lower Extremity/blood supply ; Intermittent Claudication ; Endothelial Cells ; Risk Factors
Language	English
Publishing date	2023-12-13
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms242417439
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Article ; Online: A hidden problem: peripheral artery disease in women.

Kavurma, Mary M / Boccanfuso, Lauren / Cutmore, Carina / Passam, Freda / Patel, Sanjay / Hennessy, Annemarie / Loa, Jacky / Figtree, Gemma A / Golledge, Jonathan / Robinson, David A / Aitken, Sarah

European heart journal. Quality of care & clinical outcomes

2023 Volume 9, Issue 4, Page(s) 342–350

Abstract: Peripheral artery disease (PAD) has a huge social and economic burden and is an important contributor to the global health burden. Sex differences in PAD are apparent, with recent data suggesting equal if not greater prevalence in women, and women having ...

Abstract	Peripheral artery disease (PAD) has a huge social and economic burden and is an important contributor to the global health burden. Sex differences in PAD are apparent, with recent data suggesting equal if not greater prevalence in women, and women having worse clinical outcomes. Why this occurs is not clear. To identify underlying reasons for gender inequalities in PAD, we executed a deeper exploration through a social constructive perspective. A scoping review was conducted using the World Health Organization model for analysis of gender-related needs in healthcare. Complex interacting factors, including biological, clinical, and societal variables, were reviewed to highlight gender-related inequities in the diagnosis, treatment, and management of PAD. Current gaps in knowledge were identified and insights into future directions aimed at improving these inequalities were discussed. Our findings highlight the multi-level complexities that need to be considered for strategies to improve gender-related needs in PAD healthcare.
MeSH term(s)	Female ; Humans ; Peripheral Arterial Disease/diagnosis ; Peripheral Arterial Disease/epidemiology ; Peripheral Arterial Disease/therapy
Language	English
Publishing date	2023-03-07
Publishing country	England
Document type	Review ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2823451-0
ISSN	2058-1742 ; 2058-5225
ISSN (online)	2058-1742
ISSN	2058-5225
DOI	10.1093/ehjqcco/qcad011
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Article ; Online: A "Western Diet" promotes symptoms of hepatic steatosis in spontaneously hypertensive rats.

Cartland, Siân P / Tamer, Nicole / Patil, Manisha S / Di Bartolo, Belinda A / Kavurma, Mary M

International journal of experimental pathology

2020 Volume 101, Issue 5, Page(s) 152–161

Abstract: Systemic hypertension, characterized by elevated blood pressure ≥140/90 mm Hg, is a major modifiable risk factor for cardiovascular disease. Hypertension also associates with non-alcoholic fatty liver disease (NAFLD), which is becoming common due to a ... ...

Abstract	Systemic hypertension, characterized by elevated blood pressure ≥140/90 mm Hg, is a major modifiable risk factor for cardiovascular disease. Hypertension also associates with non-alcoholic fatty liver disease (NAFLD), which is becoming common due to a modern diet and lifestyle. The aim of the present study was to examine whether a high-fat "Western" diet had effects on hypertension and associated NAFLD. Normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) were placed on a normal chow or high-fat diet for 8 weeks; blood pressure was measured fortnightly and body weight recorded weekly. As expected, SHR had elevated blood pressure compared to WKY. Diet did not influence blood pressure. Compared to SHR, WKY rats gained more weight, associating with increased white adipose tissue weight. Normotensive rats also had higher plasma cholesterol and triglycerides in response to a "Western" diet, with no changes in plasma glucose levels. Neither strain developed atherosclerosis. Interestingly, high-fat diet-fed SHR had increased liver weight, associating with a significant level of hepatic lipid accumulation not observed in WKY. Further, they exhibited hepatocellular ballooning and increased hepatic inflammation, indicative of steatohepatitis. These findings suggest that a high-fat "Western" diet promotes features of NAFLD in SHR, but not WKY rats. Importantly, the high-fat diet had no effect on blood pressure.
MeSH term(s)	Animals ; Blood Pressure ; Cholesterol/blood ; Diet, High-Fat/adverse effects ; Fatty Liver/etiology ; Fatty Liver/physiopathology ; Hypertension/complications ; Hypertension/physiopathology ; Liver/physiopathology ; Male ; Non-alcoholic Fatty Liver Disease/complications ; Non-alcoholic Fatty Liver Disease/etiology ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Triglycerides/blood
Chemical Substances	Triglycerides ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2020-08-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1016006-1
ISSN	1365-2613 ; 0958-4625 ; 0007-1021 ; 0959-9673
ISSN (online)	1365-2613
ISSN	0958-4625 ; 0007-1021 ; 0959-9673
DOI	10.1111/iep.12369
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Ud II Zs.52: Show issues

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Article: NADPH Oxidases, Angiogenesis, and Peripheral Artery Disease.

Manuneedhi Cholan, Pradeep / Cartland, Siân P / Kavurma, Mary M

Antioxidants (Basel, Switzerland)

2017 Volume 6, Issue 3

Abstract: Peripheral artery disease (PAD) is caused by narrowing of arteries in the limbs, normally occurring in the lower extremities, with severe cases resulting in amputation of the foot or leg. A potential approach for treatment is to stimulate the formation ... ...

Abstract	Peripheral artery disease (PAD) is caused by narrowing of arteries in the limbs, normally occurring in the lower extremities, with severe cases resulting in amputation of the foot or leg. A potential approach for treatment is to stimulate the formation of new blood vessels to restore blood flow to limb tissues. This is a process called angiogenesis and involves the proliferation, migration, and differentiation of endothelial cells. Angiogenesis can be stimulated by reactive oxygen species (ROS), with NADPH oxidases (NOX) being a major source of ROS in endothelial cells. This review summarizes the recent evidence implicating NOX isoforms in their ability to regulate angiogenesis in vascular endothelial cells in vitro, and in PAD in vivo. Increasing our understanding of the involvement of the NOX isoforms in promoting therapeutic angiogenesis may lead to new treatment options to slow or reverse PAD.
Language	English
Publishing date	2017-07-12
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox6030056
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Article ; Online: The walking dead: macrophage inflammation and death in atherosclerosis.

Kavurma, Mary M / Rayner, Katey J / Karunakaran, Denuja

Current opinion in lipidology

2017 Volume 28, Issue 2, Page(s) 91–98

Abstract: Purpose of review: To highlight recent studies that describe novel inflammatory and signaling mechanisms that regulate macrophage death in atherosclerosis.: Recent findings: Macrophages contribute to all stages of atherosclerosis. The traditional ... ...

Abstract	Purpose of review: To highlight recent studies that describe novel inflammatory and signaling mechanisms that regulate macrophage death in atherosclerosis. Recent findings: Macrophages contribute to all stages of atherosclerosis. The traditional dogma states that in homeostatic conditions, macrophages undergo apoptosis and are efficiently phagocytosed to be cleared by a process called efferocytosis. In advanced atherosclerosis, however, defective efferocytosis results in secondary necrosis of these uncleared apoptotic cells, which ultimately contributes to the formation of the characteristic necrotic core and the vulnerable plaque. Here, we outline the different types of lesional macrophage death: apoptosis, autophagic and the newly defined necroptosis (i.e. a type of programmed necrosis). Recent discoveries demonstrate that macrophage necroptosis directly contributes to necrotic core formation and plaque instability. Further, promoting the resolution of inflammation using preresolving mediators has been shown to enhance efferocytosis and decrease plaque vulnerability. Finally, the canonical 'don't eat me' signal CD47 has recently been described as playing an important role in atherosclerotic lesion progression by impairing efficient efferocytosis. Although we have made significant strides in improving our understanding of cell death and clearance mechanisms in atherosclerosis, there still remains unanswered questions as to how these pathways can be harnessed using therapeutics to promote lesion regression and disease stability. Summary: Improving our understanding of the mechanisms that regulate macrophage death in atherosclerosis, in particular apoptosis, necroptosis and efferocytosis, will provide novel therapeutic opportunities to resolve atherosclerosis and promote plaque stability.
Language	English
Publishing date	2017-04
Publishing country	England
Document type	Journal Article
ZDB-ID	1045394-5
ISSN	1473-6535 ; 0957-9672
ISSN (online)	1473-6535
ISSN	0957-9672
DOI	10.1097/MOL.0000000000000394
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Zs.A 3010: Show issues

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