Pressure overload induces IL-18 and IL-18R expression, but markedly suppresses IL-18BP expression in a rabbit model. IL-18 potentiates TNF-α-induced cardiomyocyte death.

@article{Yoshida2014PressureOI,
  title={Pressure overload induces IL-18 and IL-18R expression, but markedly suppresses IL-18BP expression in a rabbit model. IL-18 potentiates TNF-α-induced cardiomyocyte death.},
  author={Tadashi Yoshida and Ingeborg Friehs and Srinivas Mummidi and Pedro J. del Nido and Solange Addulnour-Nakhoul and Patrice Delafontaine and Anthony J Valente and Bysani Chandrasekar},
  journal={Journal of molecular and cellular cardiology},
  year={2014},
  volume={75},
  pages={141-51}
}
Recurrent or sustained inflammation plays a causal role in the development and progression of left ventricular hypertrophy (LVH) and its transition to failure. Interleukin (IL)-18 is a potent pro-hypertrophic inflammatory cytokine. We report that induction of pressure overload in the rabbit, by constriction of the descending thoracic aorta induces compensatory hypertrophy at 4weeks (mass/volume ratio: 1.7±0.11) and ventricular dilatation indicative of heart failure at 6weeks (mass/volume ratio… CONTINUE READING

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