Identification of Secreted Modular Calcium-Binding Protein 1 as a Novel Endogenous Protective Molecule Against Acute Myocardial Infarction–Induced Cardiac Rupture
Authors' conclusion
Our study provides the first evidence that the transient upregulation and secretion of cardiomyocyte-derived SMOC-1 constitute an intrinsic profibrotic and antirupture response to severe ischemic injury.
Study context
- Population
- Patients with acute myocardial infarction (AMI) and AMI animal models (mice)
- Comparison
- AMI with cardiac rupture vs without; cardiomyocyte-specific SMOC-1 knockout and AAV9-mediated SMOC-1 overexpression
- Outcome
- Plasma proteins altered in AMI with vs without cardiac rupture (proteomics); SMOC-1 role in post-AMI cardiac rupture
Methodological detailsunbiased proteomics, loss- and gain-of-function animal models
- Unbiased proteomics
- Loss- and gain-of-function animal models
Main finding
As reported in the abstract
Proteins significantly upregulated in AMI with vs without cardiac rupture
9
Proteins significantly downregulated in AMI with vs without cardiac rupture
24
Original publication
Identification of Secreted Modular Calcium-Binding Protein 1 as a Novel Endogenous Protective Molecule Against Acute Myocardial Infarction–Induced Cardiac Rupture. Circulation. Published 29 September 2026. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →