ReviewThe FEBS journal2023
Therapeutic opportunities for senolysis in cardiovascular disease.
Review in The FEBS journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 45 citations in OpenAlex.
- Recent Advances in Comprehending Endothelial Dysfunction and Diabetic Cardiomyopathy: From Molecular Mechanisms to Clinical Applications.Journal of cardiovascular development and disease · 2026Review
- IGFBP7 and Heart Failure: From Senescence Biomarker to Therapeutic Target.Current heart failure reports · 2026Review
- Tacrolimus Induced Hypertension and Vascular Remodeling Includes Mechanisms of Cellular Senescence-The Protective Effect of Valsartan.Acta physiologica (Oxford, England) · 2026Article
- Secretory products from regulatory macrophages modulate senescence in human endothelial cells: implications for cardiovascular aging and diseases.BMC cardiovascular disorders · 2026Article
- Myocardiocyte senescence in ischemic heart disease and breathome changes.World journal of experimental medicine · 2026Review
- The Role of Cellular Senescence and SASP in the Pathogenesis of Atherosclerosis and the Therapeutic Potential of Senolytic Strategies in Cardiovascular Diseases.Biomedicines · 2026Review
- SASP-mediated cellular senescence following myocardial infarction: from spatiotemporal immune regulation to therapeutic strategies.Frontiers in immunology · 2026Review
- The Emerging Role of Senolysis in Atherosclerosis.Medicina (Kaunas, Lithuania) · 2025Review
- Targeting Cellular Senescence: Pathophysiology in Multisystem Age-Related Diseases.Biomedicines · 2025Review
- Anti-senescence therapies: a new concept to address cardiovascular disease.Cardiovascular research · 2025Review
- Systemic aging fuels heart failure: Molecular mechanisms and therapeutic avenues.ESC heart failure · 2025Review
- Cellular senescence in age-related cardiovascular disease: past and future.Frontiers in aging · 2025Review
- Predictive Model for In-Hospital Death in Older Patients with Type 2 Diabetes Mellitus: A Multicenter Retrospective Study in Southwest China.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Aging-associated mechanisms of atrial fibrillation progression and their therapeutic potential.The journal of cardiovascular aging · 2024Article
- The potential of flavonoids to mitigate cellular senescence in cardiovascular disease.Biogerontology · 2024Review
- Identification of Prominin-2 as a new player of cardiomyocyte senescence in the aging heart.Aging cell · 2024Article
- To target cellular senescence in diabetic kidney disease: the known and the unknown.Clinical science (London, England : 1979) · 2024Review
- Novel Techniques, Biomarkers and Molecular Targets to Address Cardiometabolic Diseases.Journal of clinical medicine · 2024Review
- A high-resolution view of the heterogeneous aging endothelium.Angiogenesis · 2024Review
- Tobacco smoke condensate-induced senescence in endothelial cells was ameliorated by colchicine treatment via suppression of NF-κB and MAPKs P38 and ERK pathways activation.Cell communication and signaling : CCS · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cellular senescence within the cardiovascular system has, until recently, been understudied and unappreciated as a factor in the development of age-related cardiovascular diseases such as heart failure, myocardial infarction and atherosclerosis. This is in part due to challenges with defining senescence within post-mitotic cells such as cardiomyocytes. However, recent evidence has demonstrated senescent-like changes, including a senescence-associated secretory phenotype (SASP), in cardiomyocytes in response to ageing and cell stress. Other replicating cells, including fibroblasts and vascular smooth muscle cells, within the cardiovascular system have also been shown to undergo senescence and contribute to disease pathogenesis. These findings coupled with the emergence of senolytic therapies, to target and eliminate senescent cells, have provided fascinating new avenues for management of several age-related cardiovascular diseases with high prevalence. In this review, we discuss the role of senescent cells within the cardiovascular system and highlight the contribution of senescence cells to common cardiovascular diseases. We discuss the emerging role for senolytics in cardiovascular disease management while highlighting important aspects of senescence biology which must be clarified before the potential of senolytics can be fully realized.
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What OpenQuestion holds
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.