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Inflammation

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Atherosclerosis III: Management

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Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...

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Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...

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Updated: Apr 7, 2026

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

Cellular repressor of E1A-stimulated genes inhibits inflammation to decrease atherosclerosis in ApoE(-/-) mice.

Mingyu Sun¹, Xiaoxiang Tian², Yanxia Liu²

¹Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China; Cardiovascular Research Institute, Department of Cardiology, General Hospital of Shenyang Military Region, 83 Wenhua Road, Shenyang 110016, China.

Journal of Molecular and Cellular Cardiology

|July 13, 2015

Summary

This summary is machine-generated.

Cellular repressor of E1A-stimulated genes (CREG) inhibits macrophage inflammation in atherosclerosis by promoting autophagy. CREG may be a potential therapeutic target for treating this condition.

Keywords:

Atherosclerosis Autophagy Cellular repressor of E1A-stimulated genes (CREG)Inflammation Lysosome Macrophages

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Last Updated: Apr 7, 2026

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

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Published on: September 26, 2018

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Published on: June 12, 2019

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

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Published on: May 6, 2014

Area of Science:

Cardiovascular Biology
Immunology
Cellular Biology

Background:

Macrophage inflammation is a key driver in atherosclerosis pathogenesis.
Cellular repressor of E1A-stimulated genes (CREG) role in macrophage inflammation is not fully understood.

Purpose of the Study:

Investigate CREG's function in TNF-α induced macrophage inflammation.
Determine if CREG is a viable therapeutic target for atherosclerosis.

Main Methods:

Immunostaining and Western blotting to assess CREG expression in human atherosclerotic arteries and mouse models.
In vivo studies using ApoE(-/-) mice on high-fat diets with CREG protein supplementation.
In vitro experiments on macrophages involving TNF-α stimulation, CREG manipulation (supplementation/silencing), and autophagy inhibitors.

Main Results:

CREG expression was decreased in human atherosclerotic coronary arteries.
CREG supplementation reduced aortic atherosclerosis and inflammation in ApoE(-/-) mice.
CREG inhibited TNF-α induced macrophage inflammation by promoting autophagy via lysosome formation (cathepsin B/L).

Conclusions:

CREG plays a protective role by inhibiting inflammation and promoting autophagy.
CREG's mechanism involves lysosome formation and activation of autophagy.
CREG represents a promising therapeutic target for atherosclerosis treatment.