Key result
GARP-expressing myeloid cells drive adverse post-MI cardiac remodeling by promoting neutrophil infiltration and cardiomyocyte apoptosis.
Why the study?
Myeloid cells contribute to myocardial infarction progression, but their precise roles have not been fully elucidated.
Identification of GARP-expressing myeloid cells provides a novel mechanistic insight into post-myocardial infarction remodeling and potential therapeutic targets.
May guide targeted therapies to limit post-MI remodeling; hypothesis-generating pending human validation.
Myeloid cells are known to contribute to the progression of myocardial infarction. However, the precise roles of these cells have not been fully elucidated. Single-cell RNA sequencing analysis demonstrated a population of glycoprotein A repetition-predominant (GARP)-expressing myeloid cells (GEM cells) that were derived from heart-resident fibrocytes. GEM cells were found to regulate neutrophil infiltration and cardiomyocyte apoptosis, resulting in detrimental cardiac remodeling. Spatial transcriptomics suggests that GEM cells are also present in human infarcted myocardium.
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Tomimatsu et al. (2025) studied Myocardial infarction. GARP-expressing myeloid cells (GEM cells) was evaluated on Neutrophil infiltration, cardiomyocyte apoptosis, and cardiac remodeling. GARP-expressing myeloid cells (GEM cells) were identified as regulators of neutrophil infiltration and cardiomyocyte apoptosis, resulting in detrimental cardiac remodeling after myocardial infarction.
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