ReviewBiological reviews of the Cambridge Philosophical Society2022
New insight into dyslipidemia-induced cellular senescence in atherosclerosis.
Review in Biological reviews of the Cambridge Philosophical Society, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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
84 citing papers in PubMed, 137 citations in OpenAlex.
- Catalytic lactate-regulatory nanosystems attenuate cellular senescence for atherosclerosis amelioration.Bioactive materials · 2026Article
- USP5 Stabilizes TGFBR1 to Drive Vascular Smooth Muscle Cell Senescence and Atherosclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A compendium of circulating biomarkers of senescence in humans: Insights on mechanistic impact across health domains and modulation by therapeutic interventions.Ageing research reviews · 2026Review
- Hypertriglyceridaemia and its multifaceted mechanisms driving atherosclerotic cardiovascular disease.Lipids in health and disease · 2026Review
- Association Between Non-traditional Lipid Indices and Sarcopenia: Evidence from a Prospective Chinese Cohort Study.Current medical science · 2026Article
- Article
- Pharmacological targeting of the senescence-associated secretory phenotype in atherosclerosis: therapeutic potential of senolytics and senomorphics.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Dyslipidemia as a key nexus linking depression and aging acceleration: unraveling the mediating role of lipid accumulation product (LAP).European archives of psychiatry and clinical neuroscience · 2026Article
- The role of caveolin-1 in atherosclerosis and its molecular mechanism.Lipids in health and disease · 2026Review
- SASP-driven vascular aging: unraveling the transcriptional nexus in endothelial senescence and cardiovascular disease.Histochemistry and cell biology · 2026Review
- Cardiovascular ageing: hallmarks, signaling pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Association of a novel triglyceride-glucose and non-HDL-to-HDL cholesterol ratio (TyG-NHHR) index with cardiometabolic multimorbidity: a dual-cohort prospective study in Chinese and European adults.Journal of health, population, and nutrition · 2026Article
- From Beat to Risk: How Heart Rate Variability Predicts Arrhythmias in Type 2 Diabetes.Life (Basel, Switzerland) · 2026Review
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- Article
- Predictive value of non-fasting apolipoprotein B/apolipoprotein A-1 ratio combined with systatin C for severe coronary artery stenosis in patients who undergo coronary angiography.Journal of cardiothoracic surgery · 2026Article
- Biosacetalin (1,1-Diethoxyethane) Improves Healthy Lifespan inAntioxidants (Basel, Switzerland) · 2026Article
- Relationships Between Circulating Lipids, Lipoproteins, and Lymphocyte Subsets in the Multi-Ethnic Study of Atherosclerosis.Global heart · 2026Article
- PI3K/AKT signaling pathway: new strategies for treating atherosclerosis with plant-derived compounds.Frontiers in pharmacology · 2026Review
- Nonlinear and Age-Specific Associations Between Atherogenic Index of Plasma and Differential Cardiovascular Risk Profiles in US Adults.Cardiovascular therapeutics · 2026Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis, characterized by lipid-rich plaques in the arterial wall, is an age-related disorder and a leading cause of mortality worldwide. However, the specific mechanisms remain complex. Recently, emerging evidence has demonstrated that senescence of various types of cells, such as endothelial cells (ECs), vascular smooth muscle cells (VSMCs), macrophages, endothelial progenitor cells (EPCs), and adipose-derived mesenchymal stem cells (AMSCs) contributes to atherosclerosis. Cellular senescence and atherosclerosis share various causative stimuli, in which dyslipidemia has attracted much attention. Dyslipidemia, mainly referred to elevated plasma levels of atherogenic lipids or lipoproteins, or functional impairment of anti-atherogenic lipids or lipoproteins, plays a pivotal role both in cellular senescence and atherosclerosis. In this review, we summarize the current evidence for dyslipidemia-induced cellular senescence during atherosclerosis, with a focus on low-density lipoprotein (LDL) and its modifications, hydrolysate of triglyceride-rich lipoproteins (TRLs), and high-density lipoprotein (HDL), respectively. Furthermore, we describe the underlying mechanisms linking dyslipidemia-induced cellular senescence and atherosclerosis. Finally, we discuss the senescence-related therapeutic strategies for atherosclerosis, with special attention given to the anti-atherosclerotic effects of promising geroprotectors as well as anti-senescence effects of current lipid-lowering drugs.
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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 Socratic graph.