Apolipoprotein E in Cardiovascular Diseases: Novel Aspects of an Old-fashioned Enigma

Liehn, Elisa A.; Ponomariov, Victor; Diaconu, Rodica; Streaţă, Ioana; Ioana, Mihai; Crespo-Avilan, Gustavo E.; Hernández‐Reséndiz, Sauri; Cabrera-Fuentes, Héctor A.

doi:10.1016/j.arcmed.2018.08.008

Cited by 26 publications

(20 citation statements)

References 92 publications

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“…Apolipoprotein E. ApoE is a soluble 34-kDa glycoprotein, coded by three alleles (Mahley, 1988). ApoE is essential for the lipid metabolism (production, conversion, and clearance of lipoproteins) in all tissues and organs (Liehn et al, 2018) and is recognized for its ability to suppress atherosclerosis (Raffai, 2012). Although ApoE is synthesized mainly by liver (Kraft et al, 1989), many other cells or tissues are also able to synthesize ApoE, such as macrophages, adipocytes, smooth muscle cells, brain, and kidney (Driscoll and Getz, 1984;Zechner et al, 1991).…”

Section: Macrophage Cholesterol Effluxmentioning

confidence: 99%

“…ApoE has been shown to mediate uptake of chylomicrons, very LDL (VLDL) remnants, and ApoE-containing HDL (Liehn et al, 2018), as well as to regulate myelopoiesis (Murphy et al, 2011). ApoE is also known to regulate cellular signaling through the interaction with its receptors and heparin sulfate proteoglycans and to influence several biologic effects, including macrophage plasticity, smooth muscle cell proliferation and endothelial cell activation (Curtiss and Boisvert, 2000).…”

Section: Macrophage Cholesterol Effluxmentioning

confidence: 99%

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Targeting Foam Cell Formation in Atherosclerosis: Therapeutic Potential of Natural Products

et al. 2019

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Section: Macrophage Cholesterol Effluxmentioning

confidence: 99%

Section: Macrophage Cholesterol Effluxmentioning

confidence: 99%

Targeting Foam Cell Formation in Atherosclerosis: Therapeutic Potential of Natural Products

et al. 2019

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“…Atherosclerosis is an inflammatory disease characterized by the hardening and narrowing of an artery due to the accumulation of lipids, immune cells, ribonucleic acids and various fibrous elements [5,6,7,8]. Over time these accumulations develop into atherosclerotic plaques that can occlude blood vessels resulting in reduced blood flow and may lead to acute thrombotic complications [9,10,11,12,13,14]. Thrombotic events arise when vulnerable plaques rupture, exposing vascular structures to circulation setting off a coagulation cascade forming a thrombus [12,15].…”

Section: Overview Of Atherosclerosismentioning

confidence: 99%

Role of Macrophages in Cardioprotection

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Cabrera-Fuentes

Irei

et al. 2019

IJMS

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Cardiovascular diseases are the leading cause of mortality worldwide. It is widely known that non-resolving inflammation results in atherosclerotic conditions, which are responsible for a host of downstream pathologies including thrombosis, myocardial infarction (MI), and neurovascular events. Macrophages, as part of the innate immune response, are among the most important cell types in every stage of atherosclerosis. In this review we discuss the principles governing macrophage function in the healthy and infarcted heart. More specifically, how cardiac macrophages participate in myocardial infarction as well as cardiac repair and remodeling. The intricate balance between phenotypically heterogeneous populations of macrophages in the heart have profound and highly orchestrated effects during different phases of myocardial infarction. In the early “inflammatory” stage of MI, resident cardiac macrophages are replaced by classically activated macrophages derived from the bone marrow and spleen. And while the macrophage population shifts towards an alternatively activated phenotype, the inflammatory response subsides giving way to the “reparative/proliferative” phase. Lastly, we describe the therapeutic potential of cardiac macrophages in the context of cell-mediated cardio-protection. Promising results demonstrate innovative concepts; one employing a subset of yolk sac-derived, cardiac macrophages that have complete restorative capacity in the injured myocardium of neonatal mice, and in another example, post-conditioning of cardiac macrophages with cardiosphere-derived cells significantly improved patient’s post-MI diagnoses.

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“…In ApoE-2, the receptor-binding region is inactivated, which results in the delayed clearance of hepatic and intestinal remnant lipoproteins, hyperlipoproteinemia, and seems to be associated with a mild form of atherosclerosis progression. Whereas the structural change defined in ApoE-4 reshapes the lipid-binding site and then targets large triglyceride-rich VLDL rather than small phospholipid-rich HDL, individuals with ε4 allele show higher levels of LDL cholesterol, which favors the induction of atherosclerotic lesions [117]. Some studies have estimated that carriers of the ApoE-ԑ4 allele may have a 42% higher risk of cardiovascular disease than carriers of the ApoE-ԑ3/ԑ3 genotype; they also have a greater risk of Alzheimer’s disease, and in general the genotype is negatively associated with longevity [118,119,120].…”

Section: Influence Of Genetic Variants On Transport Management Amentioning

confidence: 99%

Vitamin E Metabolic Effects and Genetic Variants: A Challenge for Precision Nutrition in Obesity and Associated Disturbances

2018

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Vitamin E (VE) has a recognized leading role as a contributor to the protection of cell constituents from oxidative damage. However, evidence suggests that the health benefits of VE go far beyond that of an antioxidant acting in lipophilic environments. In humans, VE is channeled toward pathways dealing with lipoproteins and cholesterol, underlining its relevance in lipid handling and metabolism. In this context, both VE intake and status may be relevant in physiopathological conditions associated with disturbances in lipid metabolism or concomitant with oxidative stress, such as obesity. However, dietary reference values for VE in obese populations have not yet been defined, and VE supplementation trials show contradictory results. Therefore, a better understanding of the role of genetic variants in genes involved in VE metabolism may be crucial to exert dietary recommendations with a higher degree of precision. In particular, genetic variability should be taken into account in targets concerning VE bioavailability per se or concomitant with impaired lipoprotein transport. Genetic variants associated with impaired VE liver balance, and the handling/resolution of oxidative stress might also be relevant, but the core information that exists at present is insufficient to deliver precise recommendations.

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Apolipoprotein E in Cardiovascular Diseases: Novel Aspects of an Old-fashioned Enigma

Cited by 26 publications

References 92 publications

Targeting Foam Cell Formation in Atherosclerosis: Therapeutic Potential of Natural Products

Targeting Foam Cell Formation in Atherosclerosis: Therapeutic Potential of Natural Products

Role of Macrophages in Cardioprotection

Vitamin E Metabolic Effects and Genetic Variants: A Challenge for Precision Nutrition in Obesity and Associated Disturbances

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