ArticleAnnals of the New York Academy of Sciences2025
Mass spectrometry reveals age-dependent collagen decline in murine atria.
Article in Annals of the New York Academy of Sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Collagen gene expression is linked to aging and lifespan extension inMatrix biology plus · 2026Article
- Glyco-Architectural Remodelling of the Feline Heart: Age- and HCM-Related Insights from Lectin Histochemistry.Life (Basel, Switzerland) · 2025Article
- Mass spectrometry reveals age-dependent collagen decline in murine atria.Annals of the New York Academy of Sciences · 2025Article
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Authors and funding
5 authors.
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Abstract
The cardiac atrial extracellular matrix (ECM) is central to age-associated cardiac remodeling and subsequent decline in cardiac functioning. Despite this, the composition of the atrial ECM and how it changes with age is not yet known. This study utilized mass spectrometry to evaluate the composition of murine atria in young (12 weeks) and old (77 weeks) C57BL/6J mice. The tissue was decellularized, ECM and ECM-associated proteins were extracted with GuHCl, and proteins were deglycosylated to enable identification of glycosylated peptides. Two hundred and thirty-seven ECM and ECM-associated proteins were found to be significantly differentially expressed with age. Some proteins (MMP9, S100A9, VWA3A, CTSD, CCL8) were more than threefold increased with age, proteoglycans were modestly decreased, while the overall collagen content was markedly decreased. STRING network mapping of physical associations predicted that both PLOD3 and PDGFA interact with the collagens that decreased with age. The results suggest that the mechanism behind age-associated atrial stiffness is not due to an increase in collagen content as previously believed, but an increase in cross-linking, potentially facilitated by PLOD3. Additionally, several of the significant proteins have not previously been associated with cardiac aging and thus are potential drug targets for age-associated cardiac fibrosis and other age-associated conditions.
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Registered trials
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