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Cardiac macrophages promote diastolic dysfunction

Maarten Hulsmans1, Hendrik B Sager1, Jason D Roh2,3

  • 1Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA.

The Journal of Experimental Medicine
|January 18, 2018
PubMed

Insights

Cardiac macrophages expand in heart aging and diastolic dysfunction, promoting fibrosis. Targeting these cells, particularly their IL-10 production, can improve cardiac function and stiffness.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Cardiac Aging

Background:

  • Macrophages are key cardiac cells involved in homeostasis and disease.
  • The origin and function of cardiac macrophages in diastolic dysfunction are not fully understood.
  • Diastolic dysfunction is a common issue in cardiac aging and heart failure with preserved ejection fraction.

Purpose of the Study:

  • To investigate the role and origin of cardiac macrophages in diastolic dysfunction.
  • To explore the therapeutic potential of targeting cardiac macrophages in diastolic dysfunction.

Main Methods:

  • Analysis of cardiac macrophage density in human and mouse models of diastolic dysfunction.
  • Assessment of monocyte recruitment and hematopoiesis.
  • Evaluation of splenic 18F-FDG PET/CT imaging and echocardiography.
  • Investigating the effects of IL-10 deletion in macrophages.

Main Results:

  • Cardiac macrophages expand in humans and mice with diastolic dysfunction.
  • Macrophage expansion is linked to monocyte recruitment and increased hematopoiesis.
  • Cardiac macrophages produce IL-10, activating fibroblasts and promoting collagen deposition, leading to myocardial stiffness.
  • IL-10 deletion in macrophages improved diastolic function.

Conclusions:

  • Cardiac macrophage expansion and phenotypic changes are implicated in diastolic dysfunction and cardiac fibrosis.
  • Targeting cardiac macrophages, specifically their IL-10 signaling, presents a potential therapeutic strategy for diastolic dysfunction.

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