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Epicardial Fat: Physiological, Pathological, and Therapeutic Implications.

Juan Salazar1, Eliana Luzardo1, José Carlos Mejías1

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Epicardial fat influences cardiovascular health. Its inflammation releases adipokines, impacting insulin sensitivity and promoting atherosclerosis, highlighting its role as a disease risk factor and therapeutic target.

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Area of Science:

  • Cardiology
  • Endocrinology
  • Metabolic Research

Background:

  • Epicardial adipose tissue (EAT) is anatomically and functionally linked to coronary vasculature.
  • Dysregulation of EAT contributes to cardiovascular disease (CVD) development.
  • Proinflammatory adipokines secreted by EAT impact local and systemic metabolic processes.

Purpose of the Study:

  • To elucidate the role of epicardial fat in cardiovascular pathology.
  • To investigate the mechanisms by which EAT influences vascular function and atherosclerosis.
  • To establish EAT as a potential therapeutic target for CVD.

Main Methods:

  • Review of existing literature on epicardial fat, adipokines, and cardiovascular disease.
  • Analysis of the functional crosstalk between EAT and coronary vessels.
  • Exploration of the concept of vasocrine regulation by EAT-derived adipokines.

Main Results:

  • Epicardial fat dysfunction releases proinflammatory adipokines.
  • These adipokines decrease insulin sensitivity, reduce adiponectin, and promote vascular smooth muscle cell proliferation.
  • EAT-derived adipokines mediate vasocrine regulation, leading to vasoconstriction, arterial stiffness, and atherosclerotic plaque formation.

Conclusions:

  • Epicardial adipose tissue thickening is a significant risk factor for cardiovascular disease.
  • EAT represents a potential therapeutic target for cardiovascular pathologies.
  • EAT functions as a molecular interface in "endocrine-cardiology".