ArticleCardiovascular research2023
The longevity-associated BPIFB4 gene supports cardiac function and vascularization in ageing cardiomyopathy.
Article in Cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- The LAV-BPIFB4-Platelet-CD47 Axis: A Novel Mechanism Associated With Immune Resilience in Longevity.Aging cell · 2026Article
- Single-cell polygenic risk scores dissect cellular and molecular heterogeneity of complex human diseases.Nature biotechnology · 2026Article
- LAV-BPIFB4 reverses progeria-associated cardiac aging by restoring diastolic function and reducing senescence.International journal of biological sciences · 2026Article
- Artificial intelligence-assisted reinterpretation of preclinical progeria research suggests a hierarchical nuclear-vascular resilience framework with translational implications.International journal of biological sciences · 2026Article
- Review
- Cellular and molecular mechanisms underlying cardiovascular aging.Cellular & molecular biology letters · 2025Review
- The Mechanism and Potential Therapeutic Strategies of Vascular Aging.Aging medicine (Milton (N.S.W)) · 2025Review
- Anti-senescence therapies: a new concept to address cardiovascular disease.Cardiovascular research · 2025Review
- BPIFB4 rs4339026 A > G polymorphism impacts COPD susceptibility in the Kashi population, China.Scientific reports · 2025Article
- Review
- Immunotherapies for Aging and Age-Related Diseases: Advances, Pitfalls, and Prospects.Research (Washington, D.C.) · 2025Review
- The longevity-associated BPIFB4 gene guarantees vascular homeostasis and immune protection through platelets.GeroScience · 2024Article
- Healthy longevity-associated protein improves cardiac function in murine models of cardiomyopathy with preserved ejection fraction.Cardiovascular diabetology · 2024Article
- Hypoxic Inducible Factor Stabilization in Pericytes beyond Erythropoietin Production: The Good and the Bad.Antioxidants (Basel, Switzerland) · 2024Review
- Longevity-associated BPIFB4 gene counteracts the inflammatory signaling.Immunity & ageing : I & A · 2024Article
- The role of cardiac pericytes in health and disease: therapeutic targets for myocardial infarction.Nature reviews. Cardiology · 2024Review
- BPIFB4 and its longevity-associated haplotype protect from cardiac ischemia in humans and mice.Cell death & disease · 2023Article
- Effects of Human LAV-BPIFB4 Gene Therapy on the Epigenetic Clock and Health of Aged Mice.International journal of molecular sciences · 2023Article
- Role of noncoding RNAs in cardiac ageing.Frontiers in cardiovascular medicine · 2023Review
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 2 countries.
Funding
Abstract
aimsThe ageing heart naturally incurs a progressive decline in function and perfusion that available treatments cannot halt. However, some exceptional individuals maintain good health until the very late stage of their life due to favourable gene-environment interaction. We have previously shown that carriers of a longevity-associated variant (LAV) of the BPIFB4 gene enjoy prolonged health spans and lesser cardiovascular complications. Moreover, supplementation of LAV-BPIFB4 via an adeno-associated viral vector improves cardiovascular performance in limb ischaemia, atherosclerosis, and diabetes models. Here, we asked whether the LAV-BPIFB4 gene could address the unmet therapeutic need to delay the heart's spontaneous ageing. METHODS AND
resultsImmunohistological studies showed a remarkable reduction in vessel coverage by pericytes in failing hearts explanted from elderly patients. This defect was attenuated in patients carrying the homozygous LAV-BPIFB4 genotype. Moreover, pericytes isolated from older hearts showed low levels of BPIFB4, depressed pro-angiogenic activity, and loss of ribosome biogenesis. LAV-BPIFB4 supplementation restored pericyte function and pericyte-endothelial cell interactions through a mechanism involving the nucleolar protein nucleolin. Conversely, BPIFB4 silencing in normal pericytes mimed the heart failure pericytes. Finally, gene therapy with LAV-BPIFB4 prevented cardiac deterioration in middle-aged mice and rescued cardiac function and myocardial perfusion in older mice by improving microvasculature density and pericyte coverage.
conclusionsWe report the success of the LAV-BPIFB4 gene/protein in improving homeostatic processes in the heart's ageing. These findings open to using LAV-BPIFB4 to reverse the decline of heart performance in older people.
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Registered trials
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