TRα Protects Against Atherosclerosis in Male Mice: Identification of a Novel Anti-Inflammatory Property for TRα in Mice
Abstract
Hypothyroidism is associated with an increased occurrence of atherosclerosis, suggesting some protective role for thyroid hormones (THs). Hypercholesterolemia is one of the major risk factor to develop this disease. Here, we show that the well-known TH cholesterol lowering effect was dependent on TH nuclear receptor (TR)β liver activity. But most importantly, TRα was also shown to contribute of slowing down atherosclerosis progression via an independent mechanism. Introduction of TRα(0/0) deletion in the ApoE(-/-) background accelerated the appearance of plaques. Earlier cholesterol accumulation was detected in aorta macrophages, likely due to impaired cholesterol efflux. The IL-1β inflammatory cytokine was elevated in serum and macrophages in correlation with an activation of the AKT/nuclear factor κB pathway in these cells. Inhibition of AKT prevented inflammation and restored normal cholesterol efflux. Similar low-grade inflammation was identified in TRα(0/0) male mice. Thus, the mere absence of TRα is associated with elevated levels of cytokines likely responsible for cholesterol accumulation and atherosclerosis. This TRα protective activity should be relevant for other inflammatory pathologies.
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Mice with hepatocyte-specific deletion of Thrb have been described in Billon et al, 2014.
“Mice with hepatocyte‐specific deletion of Thrb have been described in (Billon et al, 2014).”
From An extended transcription factor regulatory network controls hepatocyte identity (2023) · cites this paper as Billon et al, 2014
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- Authors
- Billon, C., Canaple, L., Fleury, S., Deloire, A., Beylot, M., Dombrowicz, D., del Carmine, P., Samarut, J., & Gauthier, K.
- Affiliations
- Lyon 1 Université (FR)
- Inserm (FR)
- Anira-ANIPHY (P.d.C.), Faculté Rockefeller, Université Lyon 1, 69008 Lyon, France
- Corresponding author
- Gauthier, Karine
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2014-07-01
- Volume
- 155
- Issue
- 7
- Pages
- 2735-2745
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W2052383221
- Cited by
- 45
- References
- 45
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 3 · 2023: 5 · 2022: 3 · 2021: 4 · 2020: 5 · 2019: 4 · 2018: 5 · 2017: 4 · 2016: 2 · 2015: 4 · 2014: 1
- FWCI
- 3.64
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Topics
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Keywords
- thyroid receptor alpha, atherosclerosis, thyroid hormones, anti-inflammatory activity, IL-1β, AKT/NF-κB signaling, cholesterol efflux, ApoE-deficient mice, hypothyroidism, hypercholesterolemia, atherosclerotic plaque formation
- MeSH terms
- Animals, Aorta, Apolipoproteins E, Cell Nucleus, Cells, Cultured, Cholesterol, Inflammation, Macrophages, Mice, Inbred C57BL, Thyroid Hormones, Blotting, Western, Bone Marrow Transplantation, NF-kappa B, Mice, Knockout, Reverse Transcriptase Polymerase Chain Reaction, Thyroid Hormone Receptors alpha, Atherosclerosis, Proto-Oncogene Proteins c-akt, Mice, Interleukin-1beta, Mice, 129 Strain
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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What counts as a claim ›How we measure confidence ›How we check this ›
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