CL-316243 facilitates stable atherosclerotic plaque phenotypes in association with suppression of perivascular adipose tissue ferroptosis via upregulating C/EBPβ
Jiang Y., Li Y., Ma K., Guo S., Liao N., Zhou J.
Animal Study, published in Redox Biol (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Redox Biol (2026)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 42289168
- PMCID
- PMC13279912
- DOI
- 10.1016/j.redox.2026.104259
Abstract (original English)
Atherosclerotic plaque rupture is the leading cause of most acute cardiovascular events and death. However, effective treatment strategies targeting plaque stability remain elusive. Perivascular adipose tissue (PVAT) dysfunction is increasingly recognized as a contributor to vulnerable plaque, implying that elucidating and targeting its underlying mechanism could represent a novel therapeutic strategy for atherosclerosis. This study identifies ferroptosis as a critical pathological feature in PVAT of atherosclerotic artery, establishing a previously unrecognized link between PVAT dysfunction and ferroptosis. The β3-adrenoceptor agonist CL-316243 (CL) significantly suppressed ferroptotic markers in both cultured adipocytes and atherosclerotic PVAT. Furthermore, CL treatment reduced PVAT inflammation and dysfunction, as shown by histological, gene expression, and functional analyses, thereby facilitating stable plaque phenotypes, reflected in reduced necrotic core size, lower CD68 and MMP expression, and increased collagen content. Notably, the decline in ferroptosis markers correlated significantly with these phenotypic improvements. Mechanistically, C/EBPβ was identified as a direct transcriptional regulator of GPX4 through CUT&Tag and dual-luciferase reporter assays, by which the critical promoter binding motif was also identified. Subsequently, CL was shown to upregulate GPX4
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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