What question did this study set out to answer?

To review the lipoprotein transport-dependent and transport-independent mechanisms through which apolipoprotein E deficiency and genetic polymorphisms drive cardiovascular, metabolic, and neurological diseases.

August 31, 2022SHILAP Revista de lepidopterologíaOpen Access

Apolipoprotein E in Cardiometabolic and Neurological Health and Diseases

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Authors

JAJeyashree Alagarsamy AJAnja Jaeschke DHDavid Y. Hui

Discussion

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Overview

Review uncovers mechanisms linking apolipoprotein E variation to cardiometabolic and neurological disorders, highlighting lipid transport-dependent and independent pathways.

Key Points

To review the lipoprotein transport-dependent and transport-independent mechanisms through which apolipoprotein E deficiency and genetic polymorphisms drive cardiovascular, metabolic, and neurological diseases.
Synthesized molecular, physiological, and genetic findings from genetically modified mouse models and human population cohorts.
Evaluated APOE allele variations (ε2, ε3, ε4) across distinct tissues, including the liver, adipose tissue, vasculature, myeloid immune cells, and the brain.
ApoE clears atherogenic plasma lipoproteins via interactions with low-density lipoprotein (LDL) receptor family members and heparan sulfate proteoglycans.
ApoE regulates cell function independent of lipid clearance through cell-surface receptor signaling and local autocrine/paracrine actions.
ApoE deficiency and the ε4 polymorphic allele strongly associate with increased susceptibility to atherosclerosis, obesity, type 2 diabetes, and Alzheimer's disease.

Cite This Study

Alagarsamy et al. (2022) studied this question.

synapsesocial.com/papers/69d72004cd480cb7e5f50942 https://doi.org/10.3390/ijms23179892

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August 31, 2022SHILAP Revista de lepidopterologíaOpen Access

Apolipoprotein E in Cardiometabolic and Neurological Health and Diseases

View Full Paper

Ask AI

Bookmark

Authors

JAJeyashree Alagarsamy AJAnja Jaeschke DHDavid Y. Hui

Discussion

Member takes

Overview

Review uncovers mechanisms linking apolipoprotein E variation to cardiometabolic and neurological disorders, highlighting lipid transport-dependent and independent pathways.

Key Points

To review the lipoprotein transport-dependent and transport-independent mechanisms through which apolipoprotein E deficiency and genetic polymorphisms drive cardiovascular, metabolic, and neurological diseases.
Synthesized molecular, physiological, and genetic findings from genetically modified mouse models and human population cohorts.
Evaluated APOE allele variations (ε2, ε3, ε4) across distinct tissues, including the liver, adipose tissue, vasculature, myeloid immune cells, and the brain.
ApoE clears atherogenic plasma lipoproteins via interactions with low-density lipoprotein (LDL) receptor family members and heparan sulfate proteoglycans.
ApoE regulates cell function independent of lipid clearance through cell-surface receptor signaling and local autocrine/paracrine actions.
ApoE deficiency and the ε4 polymorphic allele strongly associate with increased susceptibility to atherosclerosis, obesity, type 2 diabetes, and Alzheimer's disease.

Cite This Study

Alagarsamy et al. (2022) studied this question.

synapsesocial.com/papers/69d72004cd480cb7e5f50942 https://doi.org/10.3390/ijms23179892

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