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Targeting immune-fibroblast cell communication in heart failure.

Junedh M Amrute1, Xin Luo2, Vinay Penna1

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Inflammation drives cardiac fibrosis by promoting specific fibroblast populations. Targeting interleukin-1β (IL-1β) signaling in immune cells and fibroblasts reduced fibrosis and improved heart function.

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Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Fibrosis Research

Background:

  • Inflammation and tissue fibrosis are linked to organ dysfunction, particularly in cardiac disease.
  • Molecular mechanisms of immune-fibroblast communication in human cardiac disease are poorly understood.
  • Current treatments do not directly target cardiac fibrosis.

Purpose of the Study:

  • To explore molecular mechanisms of immune-fibroblast communication in human cardiac disease.
  • To identify therapeutic targets for cardiac fibrosis.

Main Methods:

  • Multiomic single-cell gene expression, epitope mapping, and chromatin accessibility profiling in human hearts.
  • Genetic lineage tracing in vivo.
  • Assessment of mouse models for cardiac fibroblast modeling.
  • Ligand-receptor analysis and spatial transcriptomics.
  • In vivo manipulation of IL-1β signaling pathways.

Main Results:

  • Identified a disease-associated fibroblast trajectory with distinct myofibroblast and FAP/POSTN+ matrifibrocyte populations.
  • FAP+ fibroblasts contribute to the POSTN lineage.
  • In vivo mouse models better recapitulate human cardiac fibrosis than cultured cells.
  • IL-1β signaling between CCR2+ macrophages and fibroblasts drives FAP/POSTN+ fibroblast emergence.
  • Inhibition of IL-1β signaling reduced FAP/POSTN+ fibroblasts, myocardial fibrosis, and improved cardiac function.

Conclusions:

  • Interleukin-1β (IL-1β) signaling is a key mediator of immune-fibroblast communication driving cardiac fibrosis.
  • Targeting IL-1β signaling in macrophages and fibroblasts offers a therapeutic strategy for cardiac fibrosis.
  • Reducing inflammation can preserve organ function by mitigating tissue fibrosis.