Deficiency of NOD1 Improves the β-Adrenergic Modulation of Ca2+ Handling in a Mouse Model of Heart Failure

@article{ValBlasco2018DeficiencyON,
  title={Deficiency of NOD1 Improves the β-Adrenergic Modulation of Ca2+ Handling in a Mouse Model of Heart Failure},
  author={A. Val-Blasco and J. A. Navarro-Garc{\'i}a and M. Tamayo and M. J. Piedras and P. Prieto and C. Delgado and G. Ruiz-Hurtado and Laura Rozas-Romero and M. Gil-Fern{\'a}ndez and C. Zaragoza and L. Bosc{\'a} and M. Fern{\'a}ndez-Velasco},
  journal={Frontiers in Physiology},
  year={2018},
  volume={9}
}
Heart failure (HF) is a complex syndrome characterized by cardiac dysfunction, Ca2+ mishandling, and chronic activation of the innate immune system. Reduced cardiac output in HF leads to compensatory mechanisms via activation of the adrenergic nervous system. In turn, chronic adrenergic overstimulation induces pro-arrhythmic events, increasing the rate of sudden death in failing patients. Nucleotide-binding oligomerization domain-containing protein 1 (NOD1) is an innate immune modulator that… Expand
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