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Cellular Repressor of E1A-stimulated Genes, A New Potential Therapeutic Target for Atherosclerosis
Xiaoxiang Tian1, Chenghui Yan1, Yaling Han1
1Cardiovascular Research Institute and Department of Cardiology, The General Hospital of Shenyang Military Region, 83 Wenhua Road, 110840 Shenyang, China.
Insights
Cellular repressor of E1A-stimulated genes (CREG) may protect against atherosclerosis by regulating vascular cell homeostasis and inflammation. CREG modulates lysosome formation and autophagy, offering potential therapeutic benefits for this chronic inflammatory disease.
Area of Science:
- Cardiovascular Biology
- Cellular Biology
- Inflammation Research
Background:
- Atherosclerosis is a chronic inflammatory disease and a significant risk factor for cardiovascular events like coronary artery disease and stroke.
- Its pathology involves complex cellular interactions within artery walls.
Purpose of the Study:
- To investigate the role of human cellular repressor of E1A-stimulated genes (CREG) in vascular homeostasis and inflammation.
- To elucidate the mechanisms underlying CREG's potential protective effects against atherosclerosis.
Main Methods:
- Investigated CREG's effects on vascular wall cells and macrophages.
- Examined CREG's role as a secreted lysosomal protein.
- Analyzed CREG's modulation of the small GTPase Rab7 and its impact on autophagy.
Main Results:
- CREG was found to modulate vascular wall cell homeostasis and inhibit inflammation in vascular cells and macrophages.
- CREG functions as a soluble lysosomal protein regulating lysosome formation and maturation.
- CREG mediates autophagy in vascular tissue cells via Rab7 modulation.
Conclusions:
- CREG exhibits a potential protective effect against inflammation in the context of atherosclerosis.
- CREG's influence on lysosome formation presents a significant therapeutic target for atherosclerosis treatment.
Background:
Atherosclerosis is a chronic inflammatory disease and a major risk factor for several important cardiovascular events, particularly coronary artery disease and stroke. The pathological process of atherosclerosis is considered to be dynamic and complicated, involving interactions between various different cell types within arteries and the cells that migrate into the vessel wall.
Objective:
Human cellular repressor of E1A-stimulated genes (CREG) was originally identified as a transcription factor with the ability to antagonize transcriptional activation and cellular transformation induced by the adenovirus E1A oncoprotein. However, subsequent studies also identified it as a secreted glycoprotein able to sustain cellular homeostasis and withstand pathological cell and tissue damage.
Results:
We demonstrated that CREG may modulate homeostasis of vascular wall cells and inhibit inflammation of vascular tissue cells and macrophages, indicating a potential protective effect of CREG against inflammation. Mechanistically, CREG behaves like a typical soluble lysosomal protein that regulates the formation and maturation of lysosomes by modulating the small GTPase protein Rab7, to mediate autophagy in vascular tissue cells.
Conclusion:
The impact of CREG on lysosome formation may have important therapeutic significance in atherosclerosis.
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