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Oxidized phospholipids in cardiovascular disease

In this Review, Tsimikas and Witztum discuss the role of oxidized phospholipids (OxPLs) in atherosclerosis, describe the methods for measuring OxPLs on apolipoprotein B-containing lipoproteins (OxPL–apoB) and their relationship with lipoprotein(a), and discuss the clinical applications of the OxPL–apoB measurement for improving diagnosis, prognosis, risk reclassification and therapeutic interventions in patients with atherosclerotic cardiovascular disease.

Sotirios Tsimikas
Joseph L. Witztum
Reviews17 Oct 2023
Nature Reviews Cardiology

Volume: 21, P: 170-191
Author Correction: Human circulating CD24^hi marginal zone B cells produce IgM targeting atherogenic antigens and confer protection from vascular disease

Tanyaporn Pattarabanjird
Anh Tram Nguyen
Coleen A. McNamara
Amendments and Corrections24 Nov 2023
Nature Cardiovascular Research

Volume: 2, P: 1328
Author Correction: The contribution of amyloid deposition in the aortic valve to calcification and aortic stenosis

Karan Sud
Navneet Narula
Jagat Narula
Amendments and Corrections17 Feb 2023
Nature Reviews Cardiology

Volume: 20, P: 429
Publisher Correction: Oxidized phospholipids are proinflammatory and proatherogenic in hypercholesterolaemic mice

Xuchu Que
Ming-Yow Hung
Joseph L. Witztum
Amendments and Corrections16 Jul 2018
Nature

Volume: 561, P: E43
Lipoprotein(a), platelet function and cardiovascular disease

In this Review, Tsimikas and co-workers re-examine the role of lipoprotein(a) in the regulation of platelet function and propose areas for future research to define its clinical relevance for cardiovascular disease.

Harpreet S. Bhatia
Richard C. Becker
Sotirios Tsimikas
Reviews08 Nov 2023
Nature Reviews Cardiology

Volume: 21, P: 299-311
Human circulating CD24^hi marginal zone B cells produce IgM targeting atherogenic antigens and confer protection from vascular disease

By single-cell mass cytometry and adoptive transfer of B cell subtypes in mice, Pattarabanjird et al. show that human CD24^hi circulating marginal zone B cells produce IgM to atherosclerosis antigens and confer atheroprotection. Blocking CD24 increased vascular inflammation in hyperlipidemic humanized mice.

Tanyaporn Pattarabanjird
Anh Tram Nguyen
Coleen A. McNamara
Research30 Oct 2023
Nature Cardiovascular Research

Volume: 2, P: 1003-1014
Complement factor H binds malondialdehyde epitopes and protects from oxidative stress

David Weismann
Karsten Hartvigsen
Christoph J. Binder
Research05 Oct 2011
Nature

Volume: 478, P: 76-81
Oxidation-specific epitopes restrain bone formation

Atherosclerosis and osteoporosis are epidemiologically associated, and oxidation specific epitopes (OSEs), which can be neutralized by innate antibodies, are pathogenic for both. Here, the authors show that mice expressing antibody fragments targeted to OSEs are protected from the bone loss induced by high-fat diet and have increased bone mass when fed a normal diet, and that levels of innate antibodies to OSEs decrease with ageing.

Elena Ambrogini
Xuchu Que
Robert L. Jilka
ResearchOpen Access06 Jun 2018
Nature Communications

Volume: 9, P: 1-11
Oxidized phospholipids are proinflammatory and proatherogenic in hypercholesterolaemic mice

A single-chain variable fragment of the antibody E06, which binds to the phosphocholine headgroup of oxidized phospholipids, blocks the uptake of oxidized low-density lipoprotein by macrophages, and reduces inflammation and atherosclerosis in hypercholesterolaemic mice.

Xuchu Que
Ming-Yow Hung
Joseph L. Witztum
Research06 Jun 2018
Nature

Volume: 558, P: 301-306
The contribution of amyloid deposition in the aortic valve to calcification and aortic stenosis

Calcific aortic valve disease and stenosis have a complex pathogenesis, and no therapies are available that can halt or slow their progression. In this Perspective, Narula and colleagues explore a possible relationship between amyloid deposition, calcification and the development of aortic valve stenosis.

Karan Sud
Navneet Narula
Jagat Narula
Reviews09 Jan 2023
Nature Reviews Cardiology

Volume: 20, P: 418-428

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