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Chemokines in myocardial ischemia

Nikolaos G Frangogiannis1, Mark L Entman

  • 1Section of Cardiovascular Sciences, The Methodist Hospital and the DeBakey Heart Center, Baylor College of Medicine, One Baylor Plaza M/S F-602, Houston, TX 77030, USA. ngf@bcm.tmc.edu

Trends in Cardiovascular Medicine
|September 17, 2005
PubMed

Insights

Chemokines like monocyte chemoattractant protein-1 are crucial for healing heart attacks by controlling immune cells and tissue repair. Targeting these chemokines could offer new treatments for ischemic heart disease.

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Wound Healing Biology

Background:

  • Chemokine expression is elevated in healing myocardial infarcts, influencing leukocyte activity, angiogenesis, and fibrosis.
  • Monocyte chemoattractant protein-1 (CCL2) plays a significant role in infarct healing processes.
  • CXC chemokines, including CXCL8 and CXCL10, are also induced during infarct healing, affecting neutrophil activity and angiogenesis.

Purpose of the Study:

  • To investigate the role of chemokines, particularly monocyte chemoattractant protein-1 (CCL2), in the healing of myocardial infarcts.
  • To understand the functions of specific CXC chemokines like Interleukin-8 (CXCL8) and interferon-gamma-inducible protein-10 (CXCL10) in infarct repair.
  • To explore the potential of targeting chemokines for novel therapeutic strategies in ischemic heart disease.

Main Methods:

  • Utilized a mouse model of myocardial infarction to study chemokine expression and function.
  • Examined the effects of monocyte chemoattractant protein-1 deficiency on macrophage infiltration, cytokine synthesis, and ventricular remodeling.
  • Analyzed the induction and potential roles of CXC chemokines (CXCL8, CXCL10) in the context of infarct healing and angiogenesis.

Main Results:

  • Monocyte chemoattractant protein-1 knockout mice showed reduced macrophage infiltration, suppressed cytokine synthesis, delayed clearance of dead cells, and diminished ventricular remodeling.
  • Monocyte chemoattractant protein-1 deficiency was associated with decreased myofibroblast accumulation and potentially interstitial fibrosis in ischemic cardiomyopathy.
  • Interleukin-8 (CXCL8) was implicated in neutrophil recruitment and neovessel formation, while interferon-gamma-inducible protein-10 (CXCL10) appeared to regulate angiogenesis and fibrosis.

Conclusions:

  • Monocyte chemoattractant protein-1 is a key regulator of inflammatory cell infiltration, tissue repair, and adverse remodeling following myocardial infarction.
  • Specific CXC chemokines contribute to distinct aspects of infarct healing, balancing pro-angiogenic and anti-angiogenic/anti-fibrotic processes.
  • Understanding chemokine involvement in myocardial ischemia offers potential for developing targeted therapies to improve outcomes in patients with ischemic heart disease.

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