The DOI matches its Crossref record; 59 of the 59 references it cites were found in a registry or an index.
Altered Activation of Endothelial Anti- and Proapoptotic Pathways by High-Density Lipoprotein from Patients with Coronary Artery Disease: Role of High-Density Lipoprotein–Proteome Remodeling
Open accessAbstract
Background—: Endothelial dysfunction and injury are thought to play an important role in the progression of coronary artery disease (CAD). High-density lipoprotein from healthy subjects (HDL Healthy ) has been proposed to exert endothelial antiapoptotic effects that may represent an important antiatherogenic property of the lipoprotein. The present study therefore aimed to compare effects of HDL CAD and HDL Healthy on the activation of endothelial anti- and proapoptotic pathways and to determine which changes of the lipoprotein are relevant for these processes. Methods and Results—: HDL was isolated from patients with stable CAD (HDL sCAD ), an acute coronary syndrome (HDL ACS ), and healthy subjects. HDL Healthy induced expression of the endothelial antiapoptotic Bcl-2 protein Bcl-xL and reduced endothelial cell apoptosis in vitro and in apolipoprotein E–deficient mice in vivo. In contrast, HDL sCAD and HDL ACS did not inhibit endothelial apoptosis, failed to activate endothelial Bcl-xL, and stimulated endothelial proapoptotic pathways, in particular, p38-mitogen-activated protein kinase–mediated activation of the proapoptotic Bcl-2 protein tBid. Endothelial antiapoptotic effects of HDL Healthy were observed after inhibition of endothelial nitric oxide synthase and after delipidation, but not completely mimicked by apolipoprotein A-I or reconstituted HDL, suggesting an important role of the HDL proteome. HDL proteomics analyses and subsequent validations and functional characterizations suggested a reduced clusterin and increased apolipoprotein C-III content of HDL sCAD and HDL ACS as mechanisms leading to altered effects on endothelial apoptosis. Conclusions—: The present study demonstrates for the first time that HDL CAD does not activate endothelial antiapoptotic pathways, but rather stimulates potential endothelial proapoptotic pathways. HDL-proteome remodeling plays an important role for these altered functional properties of HDL. These findings provide novel insights into mechanisms leading to altered vascular effects of HDL in coronary disease.
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“Unlike HDL from healthy subjects, HDL from patients with CHD, kidney disease or diabetes mellitus have no protective vascular effects or may even cause paradoxical harmful effects [55, 56, 61, 70, 71, 75, 76].”
From HDL cholesterol: reappraisal of its clinical relevance (2017) · cites this paper as [75]
Citations
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Dysfunctional HDL and atherosclerotic cardiovascular disease
Rosenson, R. S., Brewer, H. B., Ansell, B. J., Barter, P., Chapman, M. J., Heinecke, J. W., Kontush, A., Tall, A. R., & Webb, N. R. (2016) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2015.124 · Cited by 822
Vascular contributions to cognitive impairment and dementia including Alzheimer's disease
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“ApoA-I and HDL are well established to protect endothelial function and promote endothelial repair in large peripheral vessels [48–50], and are also reported to affect activity of the innate immune system and provide antiinflammatory and antioxidant functions [48,49,51].”
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High-density lipoprotein revisited: biological functions and clinical relevance
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Metadata
- Authors
- Riwanto, M., Rohrer, L., Roschitzki, B., Besler, C., Mocharla, P., Mueller, M., Perisa, D., Heinrich, K., Altwegg, L., von Eckardstein, A., Lüscher, T. F., & Landmesser, U.
- Affiliations
- University of Zurich (CH)
- From Cardiology, Cardiovascular Center, University Hospital Zurich, Switzerland (M.R., C.B., P.M., M.M., K.H., L.A., T.F.L., U.L.); Cardiovascular Research, Institute of Physiology, University of Zurich, Switzerland (M.R., C.B., P.M., K.H., L.A., T.F.L., U.L.); Center for Integrative Human Physiology, University of Zurich, Switzerland (M.R., L.R., C.B., L.A., A.v.E., T.F.L., U.L.); Institute of Clinical Chemistry, University Hospital Zurich, Switzerland (L.R., A.v.E.); and Functional Genomics Center...
- ORCID
- Venue
- Circulation
- Published
- 2013-02-26
- Volume
- 127
- Issue
- 8
- Pages
- 891-904
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2769328074
- Cited by
- 337
- References
- 58
- Citations by year
- 2026: 8 · 2025: 10 · 2024: 10 · 2023: 11 · 2022: 25 · 2021: 22 · 2020: 19 · 2019: 35 · 2018: 30 · 2017: 29 · 2016: 26 · 2015: 42 · 2014: 41 · 2013: 29
- FWCI
- 25.46
- Type
- journal article
- Language
- en
- Open access
- green
- www.zora.uzh.ch
- Licence
- other-oa
- Locations
- Circulation (publishedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, other-oa)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, other-oa)
- Zurich Open Repository and Archive (University of Zurich)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- high-density lipoprotein, coronary artery disease, endothelial cell apoptosis, Bcl-xL, tBid, p38 MAPK, clusterin, apolipoprotein C-III, HDL proteome, endothelial dysfunction, acute coronary syndrome, ApoE-deficient mice, nitric oxide synthase, anti-apoptotic pathways
- MeSH terms
- Animals, Apolipoproteins E, Coronary Artery Disease, Endothelium, Vascular, Female, Flow Cytometry, Humans, Lipoproteins, HDL, Male, Mice, Inbred C57BL, Middle Aged, Signal Transduction, Apoptosis, Mice, Knockout, Proteome, Mice
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