Subendothelial retention of atherogenic lipoproteins in early atherosclerosis
By K. Skålén, M. Gustafsson, E. Rydberg, L. M. Hultén, O. Wiklund, T. Innerarity, Jan Boren. Nature, 2002
1,080 citations recorded by the source corpus.
Subfields: Endocrinology, Diabetes and Metabolism, Immunology, Surgery
View Paper: https://www.semanticscholar.org/paper/0f69ca0b954a1a7822064680a9fc78ab99db2b4a
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In Endocrinology, Diabetes and Metabolism
- I. Graham
- Jan Boren
- Marja-Riitta Taskinen
- M. Chapman
- Alberico L. Catapano
- Børge G. Nordestgaard
- Ronald M. Krauss
In Immunology
In Surgery
- I. Graham
- Jan Boren
- M. Chapman
- Marja-Riitta Taskinen
- Alberico L. Catapano
- Børge G. Nordestgaard
- J. Bentzon
- Jay D. Horton
Citations in the corpus
- Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel (2017, background): “The probability that LDL will be retained within the arterial intima leading to the development and growth of atherosclerotic plaque increases with increasing concentration of circulating LDL particles.(6) Because retention of LDL particles is a probabilistic event, one would expect, therefore, that”
- The vascular smooth muscle cell in arterial pathology: a cell that can take on multiple roles. (2012, background): “Intimal sulphate-rich proteoglycans are able to bind apoB100 by ionic interaction with basic amino acids, and therefore to initiate fatty streaks.(101) In contrast to fatty streaks, the fibrocellular”
- Diabetic dyslipidaemia: from basic research to clinical practice* (2003, background): “Both apoproteins can bind effectively to proteoglycans, the former via a newly identified binding segment of apo B 48 masked in apo B 100 [96] and the latter via a different domain [97].”
- The Pathology of Neoatherosclerosis in Human Coronary Implants: Bare Metal and Drug-Eluting Stents (2011, neutral): “Duration with any neoatherosclerosis, days 2,160 (1,800–2,880) 420 ( Incidence of any neoatherosclerosis 2 yrs 0/88 (0) 51/1 2 yrs, 6 yrs 17/76 (22) 13/ 6 yrs 14/33 (42) All 31/197 (16) 64/2 Incidence of foamy macrophage clusters 2 yrs 0/88 (0) 25/1 2 yrs, 6 yrs 2/76 (3) 6/ 6 yrs 3/33 (9) All 5/197 ”
- Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel (2020, background): “apoB100-binding domain of arterial wall proteoglycans greatly reduces atherogenesis.(49,50) Thus, the atherogenicity of LDL is linked to the abil-”
- Pathophysiology of Atherosclerosis (2022, background): “Although this review only summarizes the role of ECs in LDL infiltration, it is important to note that other factors, such as the glycocalyx [82], pericytes [83], the subendothelial extracellular matrix [84,85], and the role of shear stress [32], should be considered.”