ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2025
Neutrophil-secreted CHI3L1 exacerbates cardiac dysfunction and inflammation after myocardial infarction.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Carnosinylation of Cardiac Antigens Attenuates Immunogenic Responses and Improves Function in Failing Hearts.Journal of the American Heart Association · 2026Article
- SiglecF-expressing neutrophils differentiate from mature neutrophils locally in the heart after myocardial infarction.Experimental hematology · 2026Article
- TAK1 drives inflammatory fibroblast acquisition and shapes myocardial infarction responses in male mice.Nature communications · 2026Article
- Fibroblast Has2 limits acute heart failure following myocardial infarction in male mice.Physiological reports · 2025Article
- 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
- G-CSF-Induced Emergency Granulopoiesis Modulates Neutrophil Effector Function in Mice.Stem cell reviews and reports · 2025Article
- Neutrophil-secreted CHI3L1 exacerbates cardiac dysfunction and inflammation after myocardial infarction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Serum CHI3L1 levels correlate with disease activity in rheumatoid arthritis and reveal potential molecular mechanisms.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Myocardial infarction (MI) triggers acute inflammation, marked by neutrophil infiltration. Although neutrophils are central to this response, the exact role of various neutrophil-derived factors is not fully understood. Clinical studies have linked one such enigmatic factor, chitinase-3 like-1, to MI outcomes. Hence, we investigated its role in post-MI remodeling. We found that chitinase-3 like-1 (CHI3L1) is upregulated after MI and secreted by activated neutrophils but does not directly affect neutrophil activity. To assess whether increased CHI3L1 influences ventricular remodeling, we subjected mice to non-reperfused MI and administered recombinant CHI3L1. Increased CHI3L1 levels worsened ventricular remodeling. In contrast, CHI3L1-deficient mice showed reduced ventricular remodeling after MI. To explore the underlying mechanisms, we assessed interactions with other cells known to be important in ventricular remodeling. Immunoprofiling of infarcted CHI3L1-deficient mouse hearts revealed a faster decline in neutrophil and monocyte numbers, indicating quicker resolution of inflammation. These findings provide direct evidence that CHI3L1 exacerbates ventricular inflammation and remodeling following MI through gain- and loss-of-function approaches.
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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.