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  • Project 4
    Myocardial Injury and Apoptosis with Diesel Exhaust Exposure
  • Air pollution has long been associated with an increased risk of cardiovascular disease, however the exact mechanisms that underlie the pathogenesis of air pollution induced myocardial infarction remain incompletely understood.

    Although numerous studies have examined vascular effects as the primary cause of myocardial injury, only a few studies have investigated for direct toxic effects of inhaled pollutants on myocardial cells. Some of these studies have suggested an increased incidence of myocardial apoptosis and fibrosis after experimental exposure, raising the possibility that some of the arrhythmogenic and myopathic effects seen in clinical populations may ensue from direct myocardial injury. Accordingly, we propose the following specific aims:

    Aim 1: Determine whether exposure to diesel exhaust (DE) predisposes to hypertrophy, heart failure, apoptosis, fibrosis and myocardial infarction in vivo and in vitro in experimental mouse models.

    Aim 2: Determine whether CHF1/Hey2, an important regulator of myocardial hypertrophy and heart failure, affects the pathological response to diesel exhaust.

    Aim 3: Determine whether serum-borne mediators in exposed animals and patients induce myocardial toxicity and identify potential diesel exhaust-induced transcriptional mechanisms.

  • Director: Michael Chin, MD, PhD

    Key Personnel:
    Yonggang Liu, Senior Fellow, Cardiology