ArticleFASEB bioAdvances2023
Progranulin deficiency exacerbates cardiac remodeling after myocardial infarction.
Article in FASEB bioAdvances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 7 citations in OpenAlex.
- Progranulin deficiency induces premature vascular senescence and dysfunction.American journal of physiology. Heart and circulatory physiology · 2026Article
- Dynamic changes in OTULIN and progranulin levels in experimental myocardial infarction and cardiac remodeling.Histochemistry and cell biology · 2026Article
- Single-cell and machine learning-integrated bulk RNA-seq analysis reveals TKT as an oxidative stress-associated diagnostic biomarker in acute myocardial infarction.Human genomics · 2026Article
- Immune modulation promotes heart regeneration through macrophage and Granulin functions in medaka.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Time-dependent integrated tissue and circulating biomarker dynamics of spexin and progranulin in an experimental myocardial infarction model.Histochemistry and cell biology · 2026Article
- Beyond Leptin and Adiponectin: The Diverse Roles of Adipokines in the Myocardial Hypertrophic Process and Heart Failure and Their Potential Contribution in Obesity.International journal of molecular sciences · 2025Review
- The Adipokine Hypothesis of Heart Failure With a Preserved Ejection Fraction: A Novel Framework to Explain Pathogenesis and Guide Treatment.Journal of the American College of Cardiology · 2025Review
- Progranulin's Protective Mechanisms and Therapeutic Potential in Cardiovascular Disease.Cells · 2025Review
- Progranulin deficiency exacerbates cardiac remodeling after myocardial infarction.FASEB bioAdvances · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial infarction (MI) is a lethal disease that causes irreversible cardiomyocyte death and subsequent cardiovascular remodeling. We have previously shown that the administration of recombinant progranulin (PGRN) protects against myocardial ischemia and reperfusion injury. However, the post-MI role of PGRN remains unclear. In the present study, we investigated the effects of PGRN deficiency on cardiac remodeling after MI. Wild-type and PGRN-knockout mice were subjected to MI by ligation of the left coronary artery for histological, electrophysiological, and protein expression analysis. Cardiac macrophage subpopulations were analyzed by flow cytometry. Bone marrow-derived macrophages (BMDMs) were acquired and treated with LPS + IFN-γ and IL-4 to evaluate mRNA levels and phagocytic ability. PGRN expression was gradually increased in the whole heart at 1, 3, and 7 days after MI. Macrophages abundantly expressed PGRN at the border areas at 3 days post-MI. PGRN-knockout mice showed higher mortality, increased LV fibrosis, and severe arrhythmia following MI. PGRN deficiency increased the levels of CD206 and MerTK expression and macrophage infiltration in the infarcted myocardium, which was attributed to a larger subpopulation of cardiac CCR2
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