ArticleAmerican journal of physiology. Heart and circulatory physiology2011
SPARC mediates early extracellular matrix remodeling following myocardial infarction.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 84 citations in OpenAlex.
- Extracellular Vesicles in Cardiovascular Disease: Intercellular Signaling, Liquid Biopsy Biomarkers, and Therapeutic Translation.Circulation research · 2026Review
- A human ex vivo model of radiation-induced skin injury recapitulates p53-driven profibrotic response to radiotherapy.JCI insight · 2026Article
- Natural language processing of biomedical text to map and prioritize protein-disease associations in HFpEF.Computers in biology and medicine · 2026Article
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- An infusible decellularized extracellular matrix material binds to vasculature in infarcted myocardium and induces pro-reparative gene expression following acute myocardial infarction through inherent avidity and bioactive signaling.bioRxiv : the preprint server for biology · 2025Article
- Article
- Madecassoside mitigates acute myocardial infarction injury by activating the PKCB/SPARC signaling pathway.Acta pharmacologica Sinica · 2025Article
- Cardiac function and extracellular matrix morphology are altered by chronic high fat diet in Drosophila larvae.PloS one · 2025Article
- Uncovering differential gene expression between mtRNA-positive and -negative osteosarcoma cells: implications beyond mitochondrial function.Frontiers in genetics · 2025Article
- Modified mRNA-MediatedInternational journal of molecular sciences · 2024Article
- Global research trends and emerging opportunities for integrin adhesion complexes in cardiac repair: a scientometric analysis.Frontiers in cardiovascular medicine · 2024Article
- Don't go breakin' my heart: cardioprotective alterations to the mechanical and structural properties of reperfused myocardium during post-infarction inflammation.Biophysical reviews · 2023Review
- Macrophages in cardiac remodelling after myocardial infarction.Nature reviews. Cardiology · 2023Review
- Identification of Hub Genes in the Remodeling of Non-Infarcted Myocardium Following Acute Myocardial Infarction.Journal of cardiovascular development and disease · 2022Article
- Single-cell and spatial transcriptomics of the infarcted heart define the dynamic onset of the border zone in response to mechanical destabilization.Nature cardiovascular research · 2022Article
- The Role of Matrix Proteins in Cardiac Pathology.International journal of molecular sciences · 2022Review
- Full-Length Spatial Transcriptomics Reveals the Unexplored Isoform Diversity of the Myocardium Post-MI.Frontiers in genetics · 2022Article
- Sex-related differences of early cardiac functional and proteomic alterations in a rat model of myocardial ischemia.Journal of translational medicine · 2021Article
- Cardiac fibrosis.Cardiovascular research · 2021Review
- Recapitulating Cardiac Structure and Function In Vitro from Simple to Complex Engineering.Micromachines · 2021Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Secreted protein, acidic, and rich in cysteine (SPARC) is a matricellular protein that functions in the extracellular processing of newly synthesized collagen. Collagen deposition to form a scar is a key event following a myocardial infarction (MI). Because the roles of SPARC in the early post-MI setting have not been defined, we examined age-matched wild-type (WT; n=22) and SPARC-deficient (null; n=25) mice at day 3 post-MI. Day 0 WT (n=28) and null (n=20) mice served as controls. Infarct size was 52 ± 2% for WT and 47 ± 2% for SPARC null (P=NS), indicating that the MI injury was comparable in the two groups. By echocardiography, WT mice increased end-diastolic volumes from 45 ± 2 to 83 ± 5 μl (P < 0.05). SPARC null mice also increased end-diastolic volumes but to a lesser extent than WT (39 ± 3 to 63 ± 5 μl; P < 0.05 vs. day 0 controls and vs. WT day 3 MI). Ejection fraction fell post-MI in WT mice from 57 ± 2 to 19 ± 1%. The decrease in ejection fraction was attenuated in the absence of SPARC (65 ± 2 to 28 ± 2%). Fibroblasts isolated from SPARC null left ventricle (LV) showed differences in the expression of 22 genes encoding extracellular matrix and adhesion molecule genes, including fibronectin, connective tissue growth factor (CTGF; CCN2), matrix metalloproteinase-3 (MMP-3), and tissue inhibitor of metalloproteinase-2 (TIMP-2). The change in fibroblast gene expression levels was mirrored in tissue protein extracts for fibronectin, CTGF, and MMP-3 but not TIMP-2. Combined, the results of this study indicate that SPARC deletion preserves LV function at day 3 post-MI but may be detrimental for the long-term response due to impaired fibroblast activation.
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