Exercise training decreases store-operated Ca2+entry associated with metabolic syndrome and coronary atherosclerosis.

@article{Edwards2010ExerciseTD,
  title={Exercise training decreases store-operated Ca2+entry associated with metabolic syndrome and coronary atherosclerosis.},
  author={J. M. Edwards and Zachary P. Neeb and M. Alloosh and X. Long and Ian N Bratz and C. R. Peller and James P. Byrd and S. Kumar and A. Obukhov and M. Sturek},
  journal={Cardiovascular research},
  year={2010},
  volume={85 3},
  pages={
          631-40
        }
}
  • J. M. Edwards, Zachary P. Neeb, +7 authors M. Sturek
  • Published 2010
  • Medicine
  • Cardiovascular research
  • AIMS Stenting attenuates restenosis, but accelerated coronary artery disease (CAD) adjacent to the stent (peri-stent CAD) remains a concern in metabolic syndrome (MetS). Smooth muscle cell proliferation, a major mechanism of CAD, is mediated partly by myoplasmic Ca2+ dysregulation and store-operated Ca2+ entry (SOCE) via canonical transient receptor potential 1 (TRPC1) channels is proposed to play a key role. Exercise is known to prevent Ca2+ dysregulation in CAD. We tested the hypothesis that… CONTINUE READING
    Coronary artery disease in metabolic syndrome: a role for the sarcoplasmic reticulum Ca2+ ATPase

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