Neutrophil-secreted CHI3L1 exacerbates cardiac dysfunction and inflammation after myocardial infarction.

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 aft

SUBMITTER: Stephan JK 

PROVIDER: S-EPMC11963974 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature