ArticleAging cell2025
BubR1 Insufficiency Drives Transcriptomic Alterations and Pathology Associated With Cardiac Aging and Heart Failure.
Article in Aging cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Neutrophil Extracellular Traps: Potential Therapeutic Targets of Traditional Chinese Medicine and Natural Products for Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Establishment and validation of an interpretable machine learning-based predictive model for risk of post-PCI in-hospital heart failure in AIHD patients.Frontiers in cardiovascular medicine · 2026Article
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14 authors.
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Abstract
Aging is a prominent risk factor for heart disease, driving pathological cardiac changes such as hypertrophy, fibrosis, and cellular senescence. While BubR1 has been linked to systemic aging in mammalian models, its specific role in regulating cardiac aging remains unclear. Here, we investigated how BubR1 regulates heart aging and its potential contribution to the pathogenesis of cardiac disease, including heart failure. BubR1 insufficiency in mice resulted in marked cardiac hypertrophy, increased fibrosis, and elevated markers of cellular senescence. Transcriptomic profiling revealed widespread disruption in key pathways involved in cardiac function, including ion channel regulation, cytoskeletal organization, and contractile fiber dynamics. Comparative analysis with aged hearts demonstrated shared dysregulated gene networks, linking BubR1 deficiency to age-related cardiac dysfunction. Additionally, BubR1 hypomorphic hearts mirrored transcriptomic changes observed in end-stage heart failure patients, and BubR1 protein levels were found to decline with age in the heart and were also significantly reduced in rodent models of heart failure and in heart failure patients. BubR1 reduction in cardiomyocytes in vitro led to an increased expression of markers of heart failure, hypertrophy, and cytoskeletal remodeling, underscoring an essential and direct role of BubR1 in maintaining cardiomyocyte health. Overall, our data suggest that BubR1 deficiency is a feature of cardiac aging and disease in humans, and that sustaining BubR1 expression may offer a potential therapeutic strategy to mitigate age-associated cardiac decline and improve heart health in the elderly.
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