March 23, 2024Journal of Lipid ResearchOpen Access

Cholesterol trafficking to the ER leads to the activation of CaMKII/JNK/NLRP3 and promotes atherosclerosis

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Authors

MYMustafa YalçınkayaColumbia University Irving Medical Center WLWenli LiuLudong University TXTong XiaoSecond Affiliated Hospital of Xi'an Jiaotong University

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Implication

Experimental study demonstrates that Aster-B-mediated cholesterol trafficking to the ER triggers NLRP3 inflammasome activation in macrophages, highlighting a driver of atherosclerosis.

Key Points

Accumulation of cholesterol in macrophage endoplasmic reticulum via Aster-B activates the NLRP3 inflammasome through CaMKII/JNK signaling and BRCC3 deubiquitylation.
In vitro cholesterol loading and in vivo mouse assays show that blocking NLRP3 deubiquitylation or deleting Abro1 suppresses NETosis and reduces atherosclerotic plaques.
Targeting endoplasmic reticulum cholesterol transport or BRCC3 deubiquitylation may curb arterial inflammation—mouse model; further preclinical work needed.

Cite This Study

Yalcınkaya et al. (2024) studied this question.

synapsesocial.com/papers/68e72a70b6db6435876a442f https://doi.org/10.1016/j.jlr.2024.100534

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Implication

Experimental study demonstrates that Aster-B-mediated cholesterol trafficking to the ER triggers NLRP3 inflammasome activation in macrophages, highlighting a driver of atherosclerosis.

Cholesterol trafficking to the ER leads to the activation of CaMKII/JNK/NLRP3 and promotes atherosclerosis

Discussion

Member takes

Implication

Key Points

Cite This Study

Cholesterol trafficking to the ER leads to the activation of CaMKII/JNK/NLRP3 and promotes atherosclerosis

Discussion

Member takes

Implication

Key Points

Cite This Study

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