ArticleScience advances2025
Mitochondrial ROS drive foam cell formation via STAT5 signaling in atherosclerosis.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- pKa engineering of a near-infrared fluorescent probe for sensitive imaging of oxidative stress in atherosclerotic plaques.Smart molecules : open access · 2026Article
- Mesoporous Silica-Confined Ruthenium Nanozyme Motors Reprogram Redox-Inflammatory Crosstalk to Suppress Atherosclerosis via NRF2 Nuclear Translocation.Advanced healthcare materials · 2026Article
- Plaque-Hepatic Targeting Nanotherapy Disrupts the PCSK9-LOX-1 Axis to Suppress oxLDL in Atherosclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Ginkgo biloba L. in preventing cardiovascular disease: pharmacological effects, mechanism of action, and therapeutic potential.Acta pharmacologica Sinica · 2026Review
- Review
- Metabolic Reprogramming-Driven Cardiovascular Immune Damage: From Glyco-Lipotoxicity and Epigenetic Memory to Multidimensional Cross-Organ Communication Networks.International journal of molecular sciences · 2026Review
- [Dual role and therapeutic potential of TREM2 in atherosclerosis].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Review
- Estrogen deprivation induces hepatic inflammation, Indoleamine-2,3-dioxygenase 1, tryptophan catabolism, and plasma cholesterol.Scientific reports · 2026Article
- Oscillatory shear stress-driven endothelial-to-mesenchymal transition: a critical mechanical signal transduction mechanism in atherosclerosis progression.Cell death discovery · 2026Review
- STAT-Mediated Mitochondrial Regulation in Cardiovascular Diseases: Mechanistic Insights and STAT3-Focused Therapeutic Strategies.Biomolecules · 2026Review
- Interactions between neutrophil extracellular traps and macrophages: the key to inflammatory diseases.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
23 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophage-to-foam cell transition is an integral part of atherosclerotic plaque progression. Particularly, oxidized low-density lipoprotein (oxLDL) is a driving factor in foam cell formation, altering macrophage function and metabolism. The aim of our research was to understand the impact of oxLDL-induced mitochondrial reactive oxygen species on macrophage-to-foam cell differentiation. We demonstrate that macrophage oxLDL-derived superoxide modulates mitochondrial metabolic reprogramming, facilitating foam cell formation. Mechanistically, mitochondrial superoxide drives signal transducers and activators of transcription 5 (STAT5) activation, leading to reduced tricarboxylic acid cycle activity. In parallel, mitochondrial superoxide enhances chromatin accessibility at STAT5 target genes, establishing a distinct STAT5 signaling signature in foam cells ex vivo and in human and mouse plaques in vivo. Inhibition of STAT5 during atherosclerosis progression prevents the differentiation of macrophages to mature Trem2
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