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Bone marrow-derived cells contribute to fibrosis in the chronically failing heart

Po-Yin Chu1, Justin Mariani, Samara Finch

  • 1Heart Failure Research Group, Baker IDI Heart and Diabetes Institute, Central, Melbourne, VIC 8008, Australia.

The American Journal of Pathology
|February 13, 2010
PubMed

Insights

Bone marrow cells contribute to cardiac fibrosis in heart failure. Stromal-derived factor-1 (SDF-1) promotes this process, suggesting a new therapeutic target for heart disease.

Area of Science:

  • Cardiovascular Biology
  • Stem Cell Biology
  • Pathophysiology

Background:

  • Cardiac fibrosis is a hallmark of chronic heart failure.
  • The origin of fibroblasts contributing to fibrosis (native vs. bone marrow-derived) remains unclear.

Purpose of the Study:

  • To determine the contribution of bone marrow-derived cells to cardiac fibrosis in heart failure.
  • To investigate the role of stromal-derived factor-1 (SDF-1) in this process.

Main Methods:

  • Utilized a transgenic mouse model (Mst1) of dilated cardiomyopathy.
  • Assessed bone marrow-derived fibrocyte recruitment.
  • Measured myocardial expression and secretion of SDF-1 by cardiomyocytes.
  • Analyzed SDF-1 levels in human heart failure patients.

Main Results:

  • Significantly greater bone marrow-derived cell recruitment in Mst1 mice compared to controls.
  • Bone marrow cells constituted 17% of the fibroblast population in heart failure.
  • Heart failure patients exhibited elevated plasma SDF-1 levels.
  • Cardiomyocytes secrete SDF-1, which is upregulated by angiotensin II.
  • SDF-1 increased cardiac fibroblast migration by 59%.

Conclusions:

  • Bone marrow-derived cells play a significant role in cardiac fibrosis during heart failure.
  • SDF-1 is implicated as a key chemoattractant in this process.
  • Targeting SDF-1 may offer a therapeutic strategy for heart failure pathogenesis.

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