What question did this study set out to answer?

To determine the upstream regulatory role of NR4A1 in Parkin-mediated mitophagy, endothelial apoptosis, and atherosclerosis progression during high-fat exposure.

February 22, 2018Cell Stress and ChaperonesOpen Access

NR4A1 contributes to high-fat associated endothelial dysfunction by promoting CaMKII-Parkin-mitophagy pathways

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Authors

PLPei LiCapital Medical University YBYuzhi BaiYunnan Agricultural University XZXia ZhaoSichuan University

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Implication

Preclinical study demonstrates that NR4A1 drives endothelial cell death via CaMKII-Parkin mitophagy in high-fat models, highlighting a potential therapeutic target for atherosclerosis.

Key Points

To determine the upstream regulatory role of NR4A1 in Parkin-mediated mitophagy, endothelial apoptosis, and atherosclerosis progression during high-fat exposure.
Assessed aortic endothelial cells (AECs) exposed to oxidized low-density lipoprotein (ox-LDL) in vitro and isolated from high-fat-fed mice in vivo.
Evaluated endothelial apoptosis, mitochondrial integrity, and metabolic energy balance following NR4A1 loss-of-function and CaMKII-dependent Parkin activation assays.
Oxidized LDL exposure and high-fat diet elevated NR4A1 expression in AECs, which triggered mitochondrial mass depletion, energy failure, and cellular apoptosis.
NR4A1 facilitated CaMKII activation to phosphorylate and activate Parkin, driving excessive mitophagy, whereas NR4A1 deficiency prevented ox-LDL-induced endothelial apoptosis.

Cite This Study

Li et al. (2018) studied this question.

synapsesocial.com/papers/6aade5e38ee7767afd874026 https://doi.org/10.1007/s12192-018-0886-1

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Implication

Preclinical study demonstrates that NR4A1 drives endothelial cell death via CaMKII-Parkin mitophagy in high-fat models, highlighting a potential therapeutic target for atherosclerosis.

NR4A1 contributes to high-fat associated endothelial dysfunction by promoting CaMKII-Parkin-mitophagy pathways

Discussion

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Implication

Key Points

Cite This Study

NR4A1 contributes to high-fat associated endothelial dysfunction by promoting CaMKII-Parkin-mitophagy pathways

Discussion

Member takes

Implication

Key Points

Cite This Study

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