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={Jason M Edwards and Zachary P. Neeb and Mouhamad A Alloosh and Xin L Long and Ian N Bratz and Cassandra R Peller and James P Byrd and Sanjay Kumar and Alexander G Obukhov and Michael S Sturek},
  journal={Cardiovascular research},
  year={2010},
  volume={85 3},
  pages={
          631-40
        }
}
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
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