Targeted disruption of the class B scavenger receptor CD36 protects against atherosclerotic lesion development in mice.
By M. Febbraio, E. Podrez, Jonathan D. Smith, D. Hajjar, Stanley L Hazen, H. Hoff, Kavita Sharma, R. Silverstein. Journal of Clinical Investigation, 2000
1,091 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology, Surgery
View Paper: https://www.semanticscholar.org/paper/15d1b34630464ade8a86b322088d26baa64f15fa
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In Immunology
- T. Lawrence
- M. Karin
- Christopher K. Glass
- E. Latz
- V. Nizet
- K. Moore
- Katherine A. Fitzgerald
- K. Woollard
In Molecular Biology
- M. Karin
- E. Latz
- T. Lawrence
- Katherine A. Fitzgerald
- Christopher K. Glass
- Eric J. Topol
- Daniel L. Kastner
- Stanley L Hazen
In Surgery
Citations in the corpus
- Association between myeloperoxidase levels and risk of coronary artery disease. (2001, background): “Uptake occurs via the scavenger receptor CD36,(15) a receptor that appears to play a major role in foam cell formation in vivo.(36) Myeloperoxidase may thus be involved in the atherosclerotic process directly by promoting lesion development.”
- CD36, a Scavenger Receptor Involved in Immunity, Metabolism, Angiogenesis, and Behavior (2009, neutral): “atherosclerosis (32) and thrombosis (44)”
- NLRP3 inflammasome: From a danger signal sensor to a regulatory node of oxidative stress and inflammatory diseases (2015, neutral): “…. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 302 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 304”
- Monocytes in atherosclerosis: subsets and functions (2010, background): “Early studies showed that scavenger receptors are proatherogenic, on the basis that CD36 −/− apoE −/− mice were protected from atherosclerosis”
- Peroxisome proliferator–activated receptor γ ligands inhibit development of atherosclerosis in LDL receptor–deficient mice (2000, background): “In analogy, disruption of the SR-A and CD36 genes results in a significant reduction of hypercholesterolemia-induced atherosclerosis in mice (12, 13).”
- Oxidative Stress: Harms and Benefits for Human Health (2017, background): “Macrophage transition to foam cells is one of the earlier and important steps in atherosclerotic lesion formation; CD36 receptor is one of the key players involved, being a scavenger receptor responsible for oxidized-LDL (oxLDL) uptake from bloodstream [56, 57].”
- The European perspective on vitamin E: current knowledge and future research. (2002, background): “This idea is supported by the observation that disruption of CD36 protects against atherosclerotic lesion development in mice (132).”
- CD36 coordinates NLRP3 inflammasome activation by facilitating the intracellular nucleation from soluble to particulate ligands in sterile inflammation (2013, background): “In the AD brain and diabetic pancreas, amyloid plaques arise from the aggregation of pre-fibrillar amyloidogenic peptides such as the Aβ(1-42) peptide17, 18, 19 or IAPP20, 21, 22, which oligomerize and give rise to higher order structures, including fibrils.”
- Innate immunity gone awry: linking microbial infections to chronic inflammation and cancer. (2006, background): “Most likely, the major cause of persistent macrophage recruitment and activation within developing atherosclerotic plaques are oxidized forms of LDL taken up by scavenger receptors (Febbraio et al., 2000).”