Related Experiment Video

Updated: May 22, 2026

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
07:36

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

Published on: September 26, 2018

Vitamin D receptor signaling inhibits atherosclerosis in mice

Frances L Szeto1, Catherine A Reardon, Dosuk Yoon

  • 1Department of Pathology, Division of Biological Sciences, The University of Chicago, Chicago, Illinois 60637, USA.

Molecular Endocrinology (Baltimore, Md.)
|May 29, 2012
PubMed

Insights

Vitamin D receptor (VDR) signaling in macrophages suppresses atherosclerosis by inhibiting the local renin-angiotensin system (RAS). Inactivating VDR accelerates atherosclerosis, highlighting VDR

Area of Science:

  • Cardiovascular Biology
  • Endocrinology
  • Immunology

Background:

  • Vitamin D is linked to cardiovascular health, but its role in atherosclerosis via the vitamin D receptor (VDR) is understudied.
  • Atherosclerosis involves complex inflammatory processes and lipid metabolism, with potential VDR involvement.
  • The renin-angiotensin system (RAS) is implicated in cardiovascular disease, but its interaction with VDR in atherosclerosis is unclear.

Purpose of the Study:

  • To investigate the impact of vitamin D receptor (VDR) signaling inactivation on atherosclerosis development.
  • To elucidate the anti-atherosclerotic mechanisms of vitamin D, particularly in macrophages.
  • To determine the role of the renin-angiotensin system (RAS) in VDR-deficient atherosclerosis.

Main Methods:

  • Utilized genetically modified mouse models, including LDLR(-/-)/VDR(-/-) and Rag-1(-/-)/VDR(-/-) mice.
  • Employed bone marrow transplantation (BMT) studies to assess VDR function in specific cell types.
  • Administered aliskiren, a renin inhibitor, to evaluate the effect on atherosclerosis progression.

Main Results:

  • VDR inactivation in mice accelerated atherosclerosis, increasing aortic adhesion molecules and inflammatory cytokines.
  • Macrophages lacking VDR exhibited increased renin expression, and aliskiren treatment reduced atherosclerosis in VDR-deficient mice.
  • Macrophage-specific VDR signaling was critical for suppressing atherosclerosis, partly through inhibition of local RAS activation.

Conclusions:

  • Macrophage VDR signaling plays a crucial role in inhibiting atherosclerosis.
  • VDR's anti-atherosclerotic effect is mediated, in part, by suppressing the local renin-angiotensin system within macrophages.
  • Targeting VDR or RAS may offer therapeutic strategies for atherosclerosis.

More Related Videos

Quantification of Atherosclerosis in Mice06:59

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

Related Concept Videos

Atherosclerosis III: Management01:26

Atherosclerosis 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...
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR activation may...
Cholesterol: Significance and Regulation01:29

Cholesterol: Significance and Regulation

Although not a source of energy, cholesterol plays a significant role as a foundational structure for bile salts, steroid hormones, and vitamin D, as well as being a crucial component of plasma membranes. Approximately 15% of blood cholesterol is derived from our diet, with the remainder synthesized from acetyl CoA by the liver and intestines. Cholesterol is eliminated from the body through its conversion into bile salts, which are eventually discarded in the feces.
Considering cholesterol and...
Inflammation01:38

Inflammation

Overview