Extracellular Vesicles as Mediators of Pathophysiology and Disease Progression in Cardiovascular Diseases

Melina Tangos1,2, Luca Schneider1,2, Oliver Jarkas1,2

  • 1Department of Cellular and Translational Physiology, Institute of Physiology, Medical Faculty, Ruhr University Bochum, 44801 Bochum, Germany.

Insights

Extracellular vesicles (EVs) play key roles in cardiovascular diseases (CVDs) by carrying disease-specific molecules. These EVs show promise as diagnostic biomarkers and therapeutic agents for heart repair.

Area of Science:

  • Cardiovascular Research
  • Biomedical Science
  • Regenerative Medicine

Background:

  • Cardiovascular diseases (CVDs) present a growing global health and economic challenge.
  • Existing treatments face limitations, driving the need for innovative therapies.
  • Extracellular vesicles (EVs) are crucial mediators of intercellular communication.

Purpose of the Study:

  • To review the multifaceted roles of EVs in cardiovascular disease (CVD) pathogenesis.
  • To highlight recent findings (last 8 years) on EV functions in CVD.
  • To explore the diagnostic and therapeutic potential of EVs in cardiology.

Main Methods:

  • Comprehensive literature review focusing on publications from the last eight years.
  • Analysis of studies investigating extracellular vesicles (EVs) in various cardiovascular conditions.
  • Synthesis of evidence on EV molecular cargo and functional impacts.

Main Results:

  • EVs from diverse origins carry disease-specific molecular cargo (miRNAs, proteins, etc.).
  • EV cargo contributes to CVD hallmarks like inflammation, fibrosis, and cardiac remodeling.
  • EVs demonstrate potential as diagnostic/prognostic biomarkers for CVDs.
  • Preclinical studies show therapeutic promise for engineered EVs in cardiac repair.

Conclusions:

  • Extracellular vesicles (EVs) are integral to cardiovascular disease (CVD) processes.
  • EVs offer significant potential as biomarkers for CVD diagnosis and prognosis.
  • EV-based therapies represent a promising avenue for promoting cardiac repair and limiting adverse remodeling.

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