Editorials |
From the Departments of Medicine/Division of Cardiology and Physiology and Biophysics (P.P.), University of Louisville, and Jewish Hospital Heart and Lung Institute (P.P.), Louisville, Ky; and Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences (E.M.), Research Triangle Park, NC.
Correspondence to Peipei Ping, PhD, 570 South Preston St, 1st Floor North, Room 122, Cardiology Research, University of Louisville, Louisville, KY 40202-1783. E-mail ping@ntr.net
Key Words: cardioprotection kinases signal transduction
| Introduction |
|---|
In this issue of Circulation Research, Dana et
al4 report that the adenosine
A1 agonist
2-chloro-N6-cyclopentyladenosine
(CCPA) induces a late phase of preconditioning in rabbit hearts.
Twenty-four hours after the transient activation of the
adenosine A1 receptor, the
myocardium exhibited a significant rise in the activity of
p38 MAPK. The increased p38 MAPK activity was completely abolished when
the infarct-sparing effect of CCPA was abrogated by either
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