A study uncovers IL-1β signaling in cardiac fibrosis, highlighting distinct fibroblast populations and promising immunotherapy strategies for heart failure.
By Dr. Sushama R. Chaphalkar, PhD.Reviewed by Danielle Ellis, B.Sc.Oct 24 2024 Researchers have reduced scar formation and improved heart function in mice with heart failure using a monoclonal antibody .
Background Inflammation and fibrosis, key factors in heart dysfunction, are prevalent in various heart diseases, particularly myocardial infarction and cardiomyopathies. Despite its clinical significance, there remains a dearth of therapeutic strategies targeting fibrosis. While mouse models have been used to identify the subtypes of fibroblasts involved in cardiac injury, the exact fibroblast populations driving fibrosis in human hearts, along with their regulatory mechanisms, remain unclear.
In the present study, researchers used cellular indexing of transcriptomes and epitopes , multiomic sequencing, and spatial transcriptomics to analyze fibroblast populations and immune interactions in human and mouse hearts. Dynamic modeling helped to characterize fibroblast differentiation trajectories, confirmed through genetic lineage tracing in mice. Additionally, chromatin accessibility was analyzed to understand the epigenetic landscape of disease-associated fibroblasts.
Thirteen distinct fibroblast cell states were identified, notably F2 and F9 , which were enriched in heart failure after MI. F9 fibroblasts, associated with extracellular matrix remodeling and immune interactions, were implicated as a potential pathogenic state. Spatial transcriptomics indicated that different fibroblast states were localized in infarct, border, and remote myocardial zones, with F9 fibroblasts colocalizing with myeloid cells.
Heart Heart Failure Immunotherapy Antibody Cardiomyopathy Cell Chemokine Chromatin Fibroblast Fibrosis Gene Heart Disease High-Throughput Sequencing Inflammation Interleukin Monoclonal Antibody Myocardial Infarction Preclinical Receptor Scar Transcription Transcriptomics
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