ArticleCardiovascular research2015
Deriving a cardiac ageing signature to reveal MMP-9-dependent inflammatory signalling in senescence.
Article in Cardiovascular research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.
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Who cites it
76 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.
- Guidelines for measuring cardiac physiology in mice.American journal of physiology. Heart and circulatory physiology · 2018Guideline
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- Multicellular senescence programs in the aged heart.Journal of molecular and cellular cardiology plus · 2026Review
- Early Post-STEMI Cardiac Rehabilitation in the CSC-Infarct Program: Real-World Safety and Effectiveness of Individualized Training Protocols.Journal of clinical medicine · 2026Article
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- Mass spectrometry reveals age-dependent collagen decline in murine atria.Annals of the New York Academy of Sciences · 2025Article
- The efferocytosis process in aging: Supporting evidence, mechanisms, and therapeutic prospects for age-related diseases.Journal of advanced research · 2025Review
- Antioxidant Senotherapy by Natural Compounds: A Beneficial Partner in Cancer Treatment.Antioxidants (Basel, Switzerland) · 2025Review
- Bioinformatics approach reveals the critical role of inflammation-related genes in age-related hearing loss.Scientific reports · 2025Article
- Advancements in Targeting Macrophage Senescence for Age-Associated Conditions.Aging and disease · 2024Review
- At the heart of inflammation: Unravelling cardiac resident macrophage biology.Journal of cellular and molecular medicine · 2024Review
- Macrophages in cardiovascular diseases: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Macrophage senescence in health and diseases.Acta pharmaceutica Sinica. B · 2024Review
- The Expression and Molecular Mechanisms of Matrix Metalloproteinase- 9 and Vascular Endothelial Growth Factor in Renal Interstitial Fibrosis in Rats.Current molecular medicine · 2024Article
- The role of cardiac resident macrophage in cardiac aging.Aging cell · 2023Review
- CCL24/CCR3 axis plays a central role in angiotensin II-induced heart failure by stimulating M2 macrophage polarization and fibroblast activation.Cell biology and toxicology · 2023Article
- Polarizing Macrophage Functional Phenotype to Foster Cardiac Regeneration.International journal of molecular sciences · 2023Review
16 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
aimsCardiac ageing involves the progressive development of cardiac fibrosis and diastolic dysfunction coordinated by MMP-9. Here, we report a cardiac ageing signature that encompasses macrophage pro-inflammatory signalling in the left ventricle (LV) and distinguishes biological from chronological ageing. METHODS AND
resultsYoung (6-9 months), middle-aged (12-15 months), old (18-24 months), and senescent (26-34 months) mice of both C57BL/6J wild type (WT) and MMP-9 null were evaluated. Using an identified inflammatory pattern, we were able to define individual mice based on their biological, rather than chronological, age. Bcl6, Ccl24, and Il4 were the strongest inflammatory markers of the cardiac ageing signature. The decline in early-to-late LV filling ratio was most strongly predicted by Bcl6, Il1r1, Ccl24, Crp, and Cxcl13 patterns, whereas LV wall thickness was most predicted by Abcf1, Tollip, Scye1, and Mif patterns. With age, there was a linear increase in cardiac M1 macrophages and a decrease in cardiac M2 macrophages in WT mice; of which, both were prevented by MMP-9 deletion. In vitro, MMP-9 directly activated young macrophage polarization to an M1/M2 mid-transition state.
conclusionOur results define the cardiac ageing inflammatory signature and assign MMP-9 roles in mediating the inflammaging profile by indirectly and directly modifying macrophage polarization. Our results explain early mechanisms that stimulate ageing-induced cardiac fibrosis and diastolic dysfunction.
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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.