ArticleCardiovascular research2024
Serine protease inhibitor, SerpinA3n, regulates cardiac remodelling after myocardial infarction.
Article in Cardiovascular research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 18 citations in OpenAlex.
- Article
- SerpinA3 is an Endogenous TGF-β Receptor Antagonist that Attenuates Cardiac Fibroblast Activation and Fibrotic Remodeling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Serpin Superfamily in Adipose Tissue Remodeling: Molecular Drivers of Immune-Metabolic Crosstalk and Insulin Sensitivity.Biology · 2026Review
- FERPIR promotes cardiomyocyte survival and attenuates cardiac remodeling after myocardial infarction.Cell death & disease · 2026Article
- Natural polysaccharide-nucleic acid nanocomplex alleviates myocardial infarction by driving chronologically programmed macrophage polarization.Materials today. Bio · 2026Article
- Integrated Omics Approach to Delineate the Mechanisms of Doxorubicin-Induced Cardiotoxicity.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Ginsenoside Rb1 Maintains Tunneling Nanotubes between Astrocytes and Neurons To Protect Mice from Cerebral ischemia/reperfusion Injury.Neurochemical research · 2026Article
- Article
- Correlation of serum MAp44 protein concentration with degree of myocardial injury and 30-day prognosis in patients with acute myocardial infarction.American journal of translational research · 2026Article
- Hypertrophic Scarring and Keloids: Epidemiology, Molecular Pathogenesis, and Therapeutic Interventions.MedComm · 2025Review
- Acute kidney injury disrupts cardiac remodeling via SerpinA3N.bioRxiv : the preprint server for biology · 2025Article
- MK2 deficiency decreases mortality in male mice during the inflammatory phase after myocardial infarction.Physiological reports · 2025Article
- Myocardial transcriptomic and proteomic landscapes across the menopausal continuum in a murine model of chemically induced accelerated ovarian failure.Physiological genomics · 2025Article
- Role of SerpinA3 in the Pathogenesis of Graves' Orbitopathy in Orbital Fibroblasts.Investigative ophthalmology & visual science · 2025Article
- Sex-related differences in the prognostic utility of inflammatory and thrombotic cardiovascular risk markers in patients with chest pain of suspected coronary origin.International journal of cardiology. Heart & vasculature · 2025Article
- Ferroptosis and protein translation: emerging perspectives in the research of myocardial infraction.Frontiers in cardiovascular medicine · 2025Review
- Prediction Value of Initial Serum Levels of SERPINA3 in Intracranial Pressure and Long-Term Neurological Outcomes in Traumatic Brain Injury.Diagnostics (Basel, Switzerland) · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
aimsFollowing myocardial infarction (MI), the heart repairs itself via a fibrotic repair response. The degree of fibrosis is determined by the balance between deposition of extracellular matrix (ECM) by activated fibroblasts and breakdown of nascent scar tissue by proteases that are secreted predominantly by inflammatory cells. Excessive proteolytic activity and matrix turnover has been observed in human heart failure, and protease inhibitors in the injured heart regulate matrix breakdown. Serine protease inhibitors (Serpins) represent the largest and the most functionally diverse family of evolutionary conserved protease inhibitors, and levels of the specific Serpin, SerpinA3, have been strongly associated with clinical outcomes in human MI as well as non-ischaemic cardiomyopathies. Yet, the role of Serpins in regulating cardiac remodelling is poorly understood. The aim of this study was to understand the role of Serpins in regulating scar formation after MI. METHODS AND
resultsUsing a SerpinA3n conditional knockout mice model, we observed the robust expression of Serpins in the infarcted murine heart and demonstrate that genetic deletion of SerpinA3n (mouse homologue of SerpinA3) leads to increased activity of substrate proteases, poorly compacted matrix, and significantly worse post-infarct cardiac function. Single-cell transcriptomics complemented with histology in SerpinA3n-deficient animals demonstrated increased inflammation, adverse myocyte hypertrophy, and expression of pro-hypertrophic genes. Proteomic analysis of scar tissue demonstrated decreased cross-linking of ECM peptides consistent with increased proteolysis in SerpinA3n-deficient animals.
conclusionOur study demonstrates a hitherto unappreciated causal role of Serpins in regulating matrix function and post-infarct cardiac remodelling.
Indexed as
Identifiers
What OpenQuestion holds
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.