The dynamic facets of the cardiac stroma: from classical markers to omics and translational perspectives

Vittorio Picchio1, Antonella Bordin1, Erica Floris1

  • 1Department of Medical Surgical Sciences and Biotechnologies, Sapienza University of Rome Italy.

Insights

Cardiac stromal cells, once underestimated, are now recognized for their complex roles in heart repair and homeostasis. Understanding these diverse cell populations is key to developing new therapies for cardiac fibrosis and remodeling.

Area of Science:

  • Cardiology
  • Cell Biology
  • Biomedical Science

Background:

  • Cardiac stromal cells, including cardiac fibroblasts, have historically been underestimated in their roles.
  • Recent single-cell transcriptomic studies reveal significant phenotypic plasticity and diverse populations within the cardiac stroma.
  • The complexity of cardiac stromal cells in homeostasis and response to injury is increasingly recognized.

Purpose of the Study:

  • To review current phenotypical and molecular markers for identifying and classifying cardiac stromal cells.
  • To synthesize recent advances in understanding cardiac stromal cell populations.
  • To provide a foundation for developing novel therapeutic strategies for cardiac conditions.

Main Methods:

  • Review of existing literature on cardiac stromal cells.
  • Analysis of single-cell transcriptomic data.
  • Identification and classification of cell markers and populations.

Main Results:

  • The cardiac stroma comprises diverse cell populations with dynamic transcriptional profiles.
  • Phenotypic plasticity of cardiac stromal cells is evident in both homeostatic and pathological conditions.
  • New markers and classification approaches are emerging for these cell types.

Conclusions:

  • A deeper understanding of cardiac stromal cells is crucial for comprehending myocardial function.
  • Advances in characterizing these cells offer a platform for novel therapeutic interventions.
  • Targeting cardiac stromal populations may counteract cardiac fibrosis and adverse remodeling.