Related Experiment Video
Updated: Jul 17, 2026
07:36
Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
Published on: September 26, 2018
Olfactomedin 2 Promotes Atherosclerosis by Eliciting Smooth Muscle Foam Cell Formation
Ning Shi1,2, Dunpeng Cai2, Bysani Chandrasekar1
1The Research Service, Harry S. Truman Memorial Veterans' Hospital, Columbia, MO (N.S., B.C., S.-Y.C.).
Arteriosclerosis, Thrombosis, and Vascular Biology
|July 16, 2026
Summary
Olfactomedin 2 (Olfm2) promotes atherosclerosis by enhancing smooth muscle cell foam cell formation via NF-κB signaling. Reducing Olfm2 levels may offer a new therapeutic approach for treating atherosclerosis.
Area of Science:
- Vascular Biology
- Molecular Medicine
- Cardiovascular Research
Background:
- Atherosclerosis involves smooth muscle cell (SMC) dysfunction.
- Olfactomedin 2 (Olfm2) influences SMC phenotype.
- The role of Olfm2 in atherosclerosis development is not well understood.
Purpose of the Study:
- To investigate the role of Olfm2 in atherosclerosis.
- To elucidate the underlying mechanisms of Olfm2's function in SMCs.
Main Methods:
- Utilized global and SMC-specific Olfm2 knockout mouse models.
- Examined Olfm2 expression in atherosclerotic plaques and oxLDL-treated SMCs.
- Investigated Olfm2's interaction with IκBα and NF-κB signaling pathways.
Main Results:
- Olfm2 is upregulated in atherosclerotic plaques and promotes SMC foam cell formation (SFCF).
- Olfm2 deficiency reduced lipid accumulation and atherosclerotic lesions in mice.
- Olfm2 activates NF-κB signaling by interacting with IκBα, promoting SFCF.
Conclusions:
- Olfm2 is a novel regulator promoting atherosclerosis and SFCF through NF-κB activation.
- Targeting Olfm2 presents a potential therapeutic strategy for atherosclerosis.
Related Concept Videos
01:38Inflammation
Overview
01:30Atherosclerosis I: Introduction
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...
01:26Coronary Artery Disease II: Pathophysiology
Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
01:26Atherosclerosis III: Management
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...
01:30Peripheral Artery Disease I: Introduction
Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...