Key result
GARP-expressing myeloid cells promote adverse cardiac remodeling in single-cell transcriptomic profiles.
Why the study?
Therapeutic strategies targeting inflammation in cardiac remodeling have shown limited clinical benefit, necessitating a more precise understanding of myeloid cell functions.
Single-cell transcriptomics and computational approaches have identified novel disease-associated myeloid states, such as GARP-expressing myeloid cells, that drive adverse cardiac remodeling.
Supports precision targeting of myeloid subsets in HF remodeling; leaves open which populations to prioritize in trials.
Adverse cardiac remodeling involves cardiomyocyte dysfunction, fibrosis, vascular alterations, and inflammation, contributing to heart failure progression. Although myeloid cells are regulators of cardiac remodeling, therapeutic strategies targeting inflammation have shown limited clinical benefit, highlighting the need for a more precise understanding of myeloid cell functions. Recent advances in single-cell transcriptomics and computational approaches have revealed substantial heterogeneity among cardiac myeloid cells and identified multiple disease-associated myeloid states with distinct molecular and functional characteristics. These findings have shifted the field beyond conventional cell classification toward understanding how specific myeloid states emerge and influence tissue remodeling through interactions with neighboring cells. In this review, we summarize recent advances in disease-associated macrophage and neutrophil states during cardiac remodeling and highlight GARP-expressing myeloid (GEM) cells as a newly identified myeloid state that promotes adverse remodeling. Understanding how disease-associated myeloid states emerge and function within multicellular tissue environments may provide new insights into cardiac remodeling.
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Obana et al. (2026) conducted a review in Cardiac remodeling. Recent advances in single-cell transcriptomics have identified disease-associated myeloid states, such as GARP-expressing myeloid cells, that promote adverse cardiac remodeling.
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