ArticleJACC. Basic to translational science2025
Phosphoglycerate Mutase 5 Is Important Mediator for Instigating Arterial Lipid Accumulation and Aggravating Atherosclerosis.
Article in JACC. Basic to translational science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Macrophage-associated kinase signaling in atherosclerosis - a systematic review.Cell communication and signaling : CCS · 2026Pooled it
- Research progress on targeted regulatory proteins in the prevention and treatment of atherosclerosis.Frontiers in immunology · 2026Review
- Current perspectives on the pathogenesis of cerebral atherosclerosis.Journal of inflammation (London, England) · 2025Review
- Unveiling the PGAM5-ANGPTL3 Axis: Implications for Atherosclerosis Progression and Therapy.JACC. Basic to translational science · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the receptor-interacting protein kinase-3 (RIPK3)-phosphoglycerate mutase 5 (PGAM5) signaling pathway is activated in other disease models, its role in atherosclerotic lesions remains unclear. This study reveals that phosphorylated RIPK3 and PGAM5 expressions are significantly elevated within macrophages in atherosclerosis lesions of humans and mice. Overexpression of PGAM5 aggravates the atherosclerotic lesion in in vivo and in vitro models. PGAM5 knockdown in macrophages promotes angiopoietin-like 3 (ANGPTL3) gene and protein expression, reduces inflammatory factor release, and inhibits inflammation and migration in endothelial and smooth muscle cells by cellular communication. This study suggests PGAM5 as a crucial mediator in atherosclerosis and a potential therapeutic target for future treatments.
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