(Q44895988)

7 December 2017

title

Apoptosis and plaque destabilization in atherosclerosis: the role of macrophage apoptosis induced by cholesterol (English)

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7 December 2017

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Tabas I

1

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7 December 2017

publication date

1 July 2004

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Cell Death & Differentiation

7 December 2017

published in

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7 December 2017

volume

11 Suppl 1

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7 December 2017

page(s)

S12-6

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https://scigraph.springernature.com/pub.10.1038/sj.cdd.4401444

7 December 2017

exact match

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cites work

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Oxidised lipoproteins may promote inflammation through the selective delay of engulfment but not binding of apoptotic cells by macrophages.

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Localization of apoptotic macrophages at the site of plaque rupture in sudden coronary death

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ABCA1-mediated cholesterol efflux is defective in free cholesterol-loaded macrophages. Mechanism involves enhanced ABCA1 degradation in a process requiring full NPC1 activity

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Macrophage apolipoprotein A-I expression protects against atherosclerosis in ApoE-deficient mice and up-regulates ABC transporters.

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Free cholesterol loading of macrophages induces apoptosis involving the fas pathway.

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Free cholesterol loading of macrophages is associated with widespread mitochondrial dysfunction and activation of the mitochondrial apoptosis pathway

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The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues

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Cytotoxic cholesterol is generated by the hydrolysis of cytoplasmic cholesteryl ester and transported to the plasma membrane

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The endoplasmic reticulum is the site of cholesterol-induced cytotoxicity in macrophages

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Niemann-Pick C heterozygosity confers resistance to lesional necrosis and macrophage apoptosis in murine atherosclerosis

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Functional and genomic analyses reveal an essential coordination between the unfolded protein response and ER-associated degradation

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Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-beta

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Coupling of stress in the ER to activation of JNK protein kinases by transmembrane protein kinase IRE1

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ASK1 is essential for endoplasmic reticulum stress-induced neuronal cell death triggered by expanded polyglutamine repeats

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CHOP is implicated in programmed cell death in response to impaired function of the endoplasmic reticulum

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Targeted disruption of the Chop gene delays endoplasmic reticulum stress-mediated diabetes

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Regulation of the endoplasmic reticulum calcium storage during the unfolded protein response--significance in tissue ischemia?

21 January 2018

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Gadd153 sensitizes cells to endoplasmic reticulum stress by down-regulating Bcl2 and perturbing the cellular redox state

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AKT/protein kinase B regulation of BCL family members during oxysterol-induced apoptosis

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Ceramide-1-phosphate blocks apoptosis through inhibition of acid sphingomyelinase in macrophages

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Sphingosine-1-phosphate inhibits acid sphingomyelinase and blocks apoptosis in macrophages

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The response-to-retention hypothesis of atherogenesis reinforced

21 January 2018

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7 January 2021

Evidence that the death of macrophage foam cells contributes to the lipid core of atheroma

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https://api.crossref.org/works/10.1038%2FSJ.CDD.4401444

7 January 2021

Cell toxicity induced by inhibition of acyl coenzyme A:cholesterol acyltransferase and accumulation of unesterified cholesterol

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7 January 2021

Evidence that the initial up-regulation of phosphatidylcholine biosynthesis in free cholesterol-loaded macrophages is an adaptive response that prevents cholesterol-induced cellular necrosis. Proposed role of an eventual failure of this response in

1 reference

https://api.crossref.org/works/10.1038%2FSJ.CDD.4401444

7 January 2021

Oxidized low density lipoprotein inhibits macrophage apoptosis by blocking ceramide generation, thereby maintaining protein kinase B activation and Bcl-XL levels

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https://api.crossref.org/works/10.1038%2FSJ.CDD.4401444

7 January 2021

Identifiers

DOI

10.1038/SJ.CDD.4401444

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7 December 2017

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