Myocardial fibrosis and diastolic dysfunction in deoxycorticosterone acetate-salt hypertensive rats is ameliorated by the peroxisome proliferator-activated receptor-alpha activator fenofibrate, partly by suppressing inflammatory responses associated with the nuclear factor-kappa-B pathway.

@article{Ogata2004MyocardialFA,
  title={Myocardial fibrosis and diastolic dysfunction in deoxycorticosterone acetate-salt hypertensive rats is ameliorated by the peroxisome proliferator-activated receptor-alpha activator fenofibrate, partly by suppressing inflammatory responses associated with the nuclear factor-kappa-B pathway.},
  author={Takehiro Ogata and Takashi Miyauchi and S. Sakai and Masakatsu Takanashi and Yoko Irukayama-Tomobe and Iwao Yamaguchi},
  journal={Journal of the American College of Cardiology},
  year={2004},
  volume={43 8},
  pages={1481-8}
}
OBJECTIVES We sought to clarify that a peroxisome proliferator-activated receptor-alpha (PPAR-alpha) activator inhibits myocardial fibrosis and its resultant diastolic dysfunction in hypertensive heart disease, as well as to investigate whether inflammatory mediators through the nuclear factor (NF)-kappa-B pathway are involved in the effects. BACKGROUND Patients with hypertensive heart disease often have diastolic heart failure without systolic dysfunction. Meanwhile, it has been well… CONTINUE READING