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TGF-beta1 overexpression: a mechanism of diastolic filling dysfunction in the aged population

Douglas F Larson1, Rene Ingham, Cory M Alwardt

  • 1Circulatory Science Graduate Perfusion Program, Sarver Heart Center, The University of Arizona College of Medicine, Tucson, Arizona, USA. dflarson@u.arizona.edu

The Journal of Extra-Corporeal Technology
|April 21, 2004
PubMed

Insights

Aging hearts show increased fibrosis and diastolic dysfunction due to cardiac fibroblast (CF) overexpressing TGF-beta1. This leads to higher collagen content and impaired heart function in older individuals.

Area of Science:

  • Cardiovascular Science
  • Aging Research
  • Fibrosis Mechanisms

Background:

  • Cardiovascular disease prevalence rises with age.
  • Aged myocardium exhibits increased fibrosis, leading to diastolic dysfunction.
  • Cardiac fibroblast (CF) maladaptive remodeling impacts myocardial infarction survival.

Purpose of the Study:

  • To investigate the hypothesis that cardiac fibroblast (CF) dysfunction and overexpressed TGF-beta1 contribute to increased cardiac collagen and diastolic dysfunction in the aged population.
  • To explore the role of TGF-beta1 in extracellular matrix protein synthesis in aged cardiac tissues.

Main Methods:

  • RT-PCR analysis of TGF-beta1 mRNA expression in young versus aged mice cardiac fibroblasts.
  • Measurement of left ventricular stiffness using the end-diastolic pressure-volume relationship parameter, beta.
  • Quantification of myocardial collagen content in young and aged mice.

Main Results:

  • Cardiac fibroblasts from aged mice showed a 43% increase in TGF-beta1 mRNA expression compared to younger mice.
  • Left ventricular stiffness (beta) was significantly higher in aged mice (0.52 +/- 0.10 mmHg/microL) than in young mice (0.30 +/- 0.05 mmHg/microL).
  • Myocardial collagen content was elevated in aged mice (16.4 +/- 2.3%) compared to young mice (9.5 +/- 4.0% of total protein).

Conclusions:

  • Cardiac fibroblast dysregulation, characterized by overexpressed TGF-beta1, contributes to diastolic filling dysfunction in the elderly.
  • These findings suggest a potential mechanism for age-related diastolic dysfunction, crucial for managing elderly open-heart surgical patients.

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