Myeloid BAF60a deficiency alters metabolic homeostasis and exacerbates atherosclerosis

被引：2

作者：

Zhao, Yang ^{[1
,2
]}

Liu, Yuhao ^{[1
]}

Zhao, Guizhen ^{[1
]}

Lu, Haocheng ^{[1
,3
]}

Liu, Yaozhong ^{[1
]}

Xue, Chao ^{[1
]}

Chang, Ziyi ^{[1
]}

Liu, Hongyu ^{[1
]}

Deng, Yongjie ^{[1
]}

Liang, Wenying ^{[1
]}

Wang, Huilun ^{[1
]}

Rom, Oren ^{[1
,4
]}

Garcia-Barrio, Minerva T. ^{[1
]}

Zhu, Tianqing ^{[1
]}

Guo, Yanhong ^{[1
]}

Chang, Lin ^{[1
]}

Lin, Jiandie ^{[5
,6
]}

Chen, Y. Eugene ^{[1
]}

Zhang, Jifeng ^{[1
]}

机构：

[1] Univ Michigan, Cardiovasc Ctr, Med Ctr, Dept Internal Med, Ann Arbor, MI 48109 USA

[2] Univ Michigan, Med Sch, Dept Pharmacol, Ann Arbor, MI 48109 USA

[3] Southern Univ Sci & Technol, Dept Pharmacol, Shenzhen 518055, Guangdong, Peoples R China

[4] Louisiana State Univ, Hlth Sci Ctr, Dept Pathol & Translat Pathobiol, Dept Mol & Cellular Physiol, Shreveport, LA 71103 USA

[5] Univ Michigan, Med Ctr, Dept Cell & Dev Biol, Ann Arbor, MI 48109 USA

[6] Univ Michigan, Med Ctr, Dept Cell & Dev Biol, Ann Arbor, MI 48109 USA

来源：

CELL REPORTS | 2023年 / 42卷 / 10期

基金：

美国国家卫生研究院;

关键词：

CHROMATIN-REMODELING COMPLEX; SMOOTH-MUSCLE-CELLS; MITOCHONDRIAL DYSFUNCTION; MACROPHAGE POLARIZATION; TRANSCRIPTION FACTOR; ACID METABOLISM; DENDRITIC CELLS; B-CELLS; ACTIVATION; MECHANISMS;

D O I：

10.1016/j.celrep.2023.113171

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Atherosclerosis, a leading health concern, stems from the dynamic involvement of immune cells in vascular plaques. Despite its significance, the interplay between chromatin remodeling and transcriptional regulation in plaque macrophages is understudied. We discovered the reduced expression of Baf60a, a component of the switch/sucrose non-fermentable (SWI/SNF) chromatin remodeling complex, in macrophages from advanced plaques. Myeloid-specific Baf60a deletion compromised mitochondrial integrity and heightened adhesion, apoptosis, and plaque development. BAF60a preserves mitochondrial energy homeostasis under pro-atherogenic stimuli by retaining nuclear respiratory factor 1 (NRF1) accessibility at critical genes. Over expression of BAF60a rescued mitochondrial dysfunction in an NRF1-dependent manner. This study illuminates the BAF60a-NRF1 axis as a mitochondrial function modulator in atherosclerosis, proposing the rejuvenation of perturbed chromatin remodeling machinery as a potential therapeutic target.

引用

页数：26

共 24 条

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