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ATF3 in atherosclerosis: a controversial transcription factor

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Abstract

Atherosclerosis, the pathophysiological basis of most malignant cardiovascular diseases, remains a global concern. Transcription factors play a key role in regulating cell function and disease progression in developmental signaling pathways involved in atherosclerosis. Activated transcription factor (ATF) 3 is an adaptive response gene in the ATF/cAMP response element binding (CREB) protein family that acts as a transcription suppressor or activator by forming homodimers or heterodimers with other ATF/CREB members. Appropriate ATF3 expression is vital for normal physiological cell function. Notably, ATF3 exhibits distinct roles in vascular endothelial cells, macrophages, and the liver, which will also be described in detail. This review provides a new perspective for atherosclerosis therapy by summarizing the mechanism of ATF3 in atherosclerosis, as well as the structure and pathophysiological properties of ATF3.

Key messages

• In endothelial cells, ATF3 overexpression aggravates oxidative stress and inflammation.

• In macrophages and liver cells, ATF3 can act as a negative regulator of inflammation and promote cholesterol metabolism.

• ATF3 can be used as a potential therapeutic factor in the treatment of atherosclerosis.

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Abbreviations

ALK:

Activin receptor-like kinase

ATF:

Activated transcription factor

Ang II:

Angiotensin II

ACE2:

Angiotensin-converting enzyme 2

AS:

Atherosclerosis

bZip:

Basic region leucine zipper

cAMP:

Cyclic adenosine monophosphate

CDK:

Cyclin-dependent kinases

CHOP:

C/EBP homologous protein

ChREBP:

Carbohydrate response element binding protein

CREB:

CAMP response element binding

CREM:

CAMP response element modulator

Clec4e:

C-type Lectin receptor 4e

CYP8B1:

Cholesterol 12α -hydroxylase

EndMT:

Endothelial-mesenchymal transition

EC:

Endothelial cell

HAEC:

Human aortic endothelial cells

HBMECs:

Human brain microvascular endothelial cells

HCAECs:

Human coronary artery endothelial cells

HDL:

High-density lipoprotein

HCD:

High-cholesterol diet

Hif:

Hypoxia inducible factor

HO-1:

Heme oxygenase-1

HUVECs:

Human umbilical vein endothelial cells

IL-6:

Interleukin-6

Ire1:

Inositol-requiring transmembrane kinase/endonuclease 1

IRF7:

IFN regulatory factor 7

I/R:

Ischemia/Reperfusion

JNK:

C-Jun N-terminal kinase

LOX1R:

Lectin-like oxidized LDL receptor 1

MMP:

Matrix metalloproteinase

NO:

Nitric oxide

NRF2:

Nuclear factor erythroid 2-related factor 2

oxLDL:

Oxidized low-density lipoprotein

PI3K/AKT:

Phosphatidylinositol-4,5-bisphosphate 3-kinase/ protein kinase B

PLGF:

Placental growth factor

rECs:

Rabbit endothelial cells

Rock1/2:

Rho-associated, coiled-coil containing protein kinase 1 and 2

Scd1:

Stearoyl-CoA desaturase 1

SAPK:

Stress-activated protein kinase

SMC:

Smooth muscle cell

SR-B1:

Scavenger receptors B1

SUMO:

Small Ubiquitin-like Modifier

TNF-α:

Tumor necrosis factor-α

TGF-β:

Transforming growth factor-β

TGRL:

Triglyceride-rich lipoproteins

TLR:

Toll-like receptor

TL:

TGRL lipolysis products

TDB:

D-( +)-trehalose 6,6'-dibehenate

VSMCs:

Vascular smooth muscle cells

VEGF:

Vascular endothelial growth factor

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Funding

This work was supported by grants from the Ningbo Natural Science Foundation of China (2019A610341).

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Authors and Affiliations

  1. Department of Cardiovascular, Medical College, Ningbo University, Ningbo, China

    Bingyu Wang, Xi Yang, Xinyi Sun, Yin Fu, Jun Qiu, Jiangfang Lian & Jianqing Zhou

  2. Department of Cardiovascular, Lihuili Hospital Affiliated to Ningbo University, Ningbo, China

    Xi Yang, Jianhui Liu, Jiangfang Lian & Jianqing Zhou

  3. Central Laboratory, Ningbo Institute of Innovation for Combined Medicine and Engineering, Ningbo, China

    Xi Yang, Jianhui Liu, Bingyang Liu, Jiangfang Lian & Jianqing Zhou

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  1. Bingyu Wang
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  2. Xi Yang
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BYW and JQZ designed the manuscript. BYW wrote the manuscript. JQ, BYL, and XYS revised the manuscript. JFL and FY revised the tables. JHL and XY revised the figures. All authors approved the manuscript for publication.

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Correspondence to Jianqing Zhou.

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Wang, B., Yang, X., Sun, X. et al. ATF3 in atherosclerosis: a controversial transcription factor. J Mol Med 100, 1557–1568 (2022). https://doi.org/10.1007/s00109-022-02263-7

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