ArticleExperimental gerontology2018
The impact of SPARC on age-related cardiac dysfunction and fibrosis in Drosophila.
Article in Experimental gerontology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Drosophila melanogaster: an old and future ally to radiobiology.Journal of radiation research · 2025Review
- Article
- Metabolic regulation of immunological aging.Nature aging · 2025Review
- SARS-CoV-2 Nsp6-Omicron causes less damage to the Drosophila heart and mouse cardiomyocytes than ancestral Nsp6.Communications biology · 2024Article
- How does a fly die? Insights into ageing from the pathophysiology of Drosophila mortality.GeroScience · 2024Review
- Distinct roles of COMPASS subunits to Drosophila heart development.Biology open · 2024Article
- Distinct Roles for COMPASS Core Subunits Set1, Trx, and Trr in the Epigenetic Regulation ofInternational journal of molecular sciences · 2023Article
- Reduction of SPARC protects mice against NLRP3 inflammasome activation and obesity.The Journal of clinical investigation · 2023Article
- H3K36 Di-Methylation Marks, Mediated by Ash1 in Complex with Caf1-55 and MRG15, Are Required duringJournal of cardiovascular development and disease · 2023Article
- What do we mean by "aging"? Questions and perspectives revealed by studies in Drosophila.Mechanisms of ageing and development · 2023Article
- Deacetylase-dependent and -independent role of HDAC3 in cardiomyopathy.Journal of cellular physiology · 2023Article
- Neprilysins regulate muscle contraction and heart function via cleavage of SERCA-inhibitory micropeptides.Nature communications · 2022Article
- Loxl2 is a mediator of cardiac aging in Drosophila melanogaster, genetically examining the role of aging clock genes.G3 (Bethesda, Md.) · 2022Article
- A Novel miRNA Screen Identifies miRNA-4454 as a Candidate Biomarker for Ventricular Fibrosis in Patients with Hypertrophic Cardiomyopathy.Biomolecules · 2021Article
- ELAC2/RNaseZ-linked cardiac hypertrophy in Drosophila melanogaster.Disease models & mechanisms · 2021Article
- Anti-Fibrotic Activity of an Antimicrobial Peptide in a Drosophila Model.Journal of innate immunity · 2021Article
- Extracellular matrix induced by steroids and aging through a G-protein-coupled receptor in aDisease models & mechanisms · 2020Article
- Myocardial fibrosis, inflammation, and altered cardiac gene expression profiles in rats exposed to a predator-based model of posttraumatic stress disorder.Stress (Amsterdam, Netherlands) · 2020Article
- As time flies by: Investigating cardiac aging in the short-lived Drosophila model.Biochimica et biophysica acta. Molecular basis of disease · 2019Review
- Organelle aging: Lessons from model organisms.Journal of genetics and genomics = Yi chuan xue bao · 2019Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Tissue fibrosis, an accumulation of extracellular matrix proteins such as collagen, accompanies cardiac ageing in humans and this is linked to an increased risk of cardiac failure. The mechanisms driving age-related tissue fibrosis and cardiac dysfunction are unclear, yet clinically important. Drosophila is amenable to the study of cardiac ageing as well as collagen deposition; however it is unclear whether collagen accumulates in the ageing Drosophila heart. This work examined collagen deposition and cardiac function in ageing Drosophila, in the context of reduced expression of collagen-interacting protein SPARC (Secreted Protein Acidic and Rich in Cysteine) an evolutionarily conserved protein linked with fibrosis. Heart function was measured using high frame rate videomicroscopy. Collagen deposition was monitored using a fluorescently-tagged collagen IV reporter (encoded by the Viking gene) and staining of the cardiac collagen, Pericardin. The Drosophila heart accumulated collagen IV and Pericardin as flies aged. Associated with this was a decline in cardiac function. SPARC heterozygous flies lived longer than controls and showed little to no age-related cardiac dysfunction. As flies of both genotypes aged, cardiac levels of collagen IV (Viking) and Pericardin increased similarly. Over-expression of SPARC caused cardiomyopathy and increased Pericardin deposition. The findings demonstrate that, like humans, the Drosophila heart develops a fibrosis-like phenotype as it ages. Although having no gross impact on collagen accumulation, reduced SPARC expression extended Drosophila lifespan and cardiac health span. It is proposed that cardiac fibrosis in humans may develop due to the activation of conserved mechanisms and that SPARC may mediate cardiac ageing by mechanisms more subtle than gross accumulation of collagen.
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