Disease-associated myeloid states in cardiac remodeling: A new era of cardiac inflammation research enabled by computational biology.
4 affiliations
- 1Laboratory of Clinical Science and Biomedicine, Graduate School of Pharmaceutical Sciences, The University of Osaka, Osaka, Japan.
- 2Laboratory of Cardiovascular Science and Drug Discovery, Graduate School of Pharmaceutical Sciences, The University of Osaka, Japan.
- 3Laboratory of Cardiovascular Science and Drug Discovery, Graduate School of Pharmaceutical Sciences, The University of Osaka, Japan; Center for Infectious Disease Education and Research, The University of Osaka (CiDER), Japan.
- 4Laboratory of Clinical Science and Biomedicine, Graduate School of Pharmaceutical Sciences, The University of Osaka, Osaka, Japan; Institute for Open and Transdisciplinary Research Initiatives (OTRI), The University of Osaka, Japan; Center for Infectious Disease Education and Research, The University of Osaka (CiDER), Japan.
Abstract
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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BibTeX
@article{obana2026diseaseassociated,
title = {{Disease-associated myeloid states in cardiac remodeling: A new era of cardiac inflammation research enabled by computational biology.}},
author = {Masanori Obana and Masashi Tomimatsu and Shota Tanaka and Keisuke Shirakura and Yoshiaki Okada and Yasushi Fujio},
journal = {The journal of physiological sciences : JPS},
year = {2026},
month = oct,
doi = {10.1016/j.jphyss.2026.100107},
url = {https://europepmc.org/article/MED/42874136},
note = {CC BY},
}
RIS
TY - JOUR
TI - Disease-associated myeloid states in cardiac remodeling: A new era of cardiac inflammation research enabled by computational biology.
AU - Masanori Obana
AU - Masashi Tomimatsu
AU - Shota Tanaka
AU - Keisuke Shirakura
AU - Yoshiaki Okada
AU - Yasushi Fujio
PY - 2026
DA - 2026/10/10
JO - The journal of physiological sciences : JPS
DO - 10.1016/j.jphyss.2026.100107
UR - https://europepmc.org/article/MED/42874136
AB - 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.
SN - 1880-6546
SN - 1880-6562
ER -