ArticleJCI insight2024
Treatment of advanced atherosclerotic mice with ABT-263 reduced indices of plaque stability and increased mortality.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 21 citations in OpenAlex.
- Intracranial aneurysms as a manifestation of premature vascular aging: Cellular senescence, inflammaging, and wall degeneration.Ageing research reviews · 2026Review
- Pharmacological targeting of the senescence-associated secretory phenotype in atherosclerosis: therapeutic potential of senolytics and senomorphics.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Epigenetic dynamics of cellular senescence: From mechanistic insights to precision senotherapy.Chinese medical journal · 2026Review
- Progranulin deficiency induces premature vascular senescence and dysfunction.American journal of physiology. Heart and circulatory physiology · 2026Article
- The right time, the right cell: the potential for precision senotherapy in pulmonary arterial hypertension.American journal of physiology. Lung cellular and molecular physiology · 2026Review
- High-Salt Diet-Induced Endothelial Dysfunction Is Mediated by Cellular Senescence.Journal of the American Heart Association · 2026Article
- Endothelial to mesenchymal transition in cardiovascular diseases: molecular insights and clinical perspectives.European heart journal · 2026Review
- Comparative analysis of senolytic drugs reveals mitochondrial determinants of efficacy and resistance.Nature aging · 2026Article
- The Role of Cellular Senescence and SASP in the Pathogenesis of Atherosclerosis and the Therapeutic Potential of Senolytic Strategies in Cardiovascular Diseases.Biomedicines · 2026Review
- Review
- Cellular Senescence, Inflammaging and Cardiovascular Disease.Immunological reviews · 2026Review
- Real-Time Monitoring of Atherosclerotic Plaque Using β-Galactosidase-Activated Photoacoustic Tomography.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- Roadmap for alleviating the manifestations of ageing in the cardiovascular system.Nature reviews. Cardiology · 2025Review
- The context-dependent effect of cellular senescence: From embryogenesis and wound healing to aging.Ageing research reviews · 2025Review
- Vascular senescence and aging: mechanisms, clinical implications, and therapeutic prospects.Biogerontology · 2025Review
- Is Senolytic Therapy in Cardiovascular Diseases Ready for Translation to Clinics?Biomolecules · 2025Review
- Mechanisms of cellular senescence-induced vascular aging: evidence of senotherapeutic strategies.The journal of cardiovascular aging · 2025Article
- Cellular senescence as a key contributor to secondary neurodegeneration in traumatic brain injury and stroke.Translational neurodegeneration · 2024Review
- Cell senescence in cardiometabolic diseases.npj aging · 2024Review
- A Conversation with ChatGPT on Contentious Issues in Senescence and Cancer Research.Molecular pharmacology · 2024Article
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Abstract
The use of senolytic agents to remove senescent cells from atherosclerotic lesions is controversial. A common limitation of previous studies is the failure to rigorously define the effects of senolytic agent ABT-263 (Navitoclax) on smooth muscle cells (SMC) despite studies claiming that these cells are the major source of senescent cells. Moreover, there are no studies on the effect of ABT-263 on endothelial cells (EC), which - along with SMC - comprise 90% of α-smooth muscle actin+ (α-SMA+) myofibroblast-like cells in the protective fibrous cap. Here we tested the hypothesis that treatment of advanced atherosclerotic mice with ABT-263 will reduce lesion size and increase plaque stability. SMC (Myh11-CreERT2-eYFP) and EC (Cdh5-CreERT2-eYFP) lineage tracing Apoe-/- mice were fed a western diet (WD) for 18 weeks, followed by ABT-263 at 100 mg/kg/bw for 6 weeks or 50 mg/kg/bw for 9 weeks. ABT-263 treatment did not change lesion size or lumen area of the brachiocephalic artery (BCA). However, ABT-263 treatment reduced SMC by 90% and increased EC contributions to lesions via EC-to-mesenchymal transition (EndoMT) by 60%. ABT-263 treatment also reduced α-SMA+ fibrous cap thickness by 60% and was associated with a > 50% mortality rate. Taken together, ABT-263 treatment of WD-fed Apoe-/- mice with advanced lesions resulted in multiple detrimental changes, including reduced indices of stability and increased mortality.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.