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|Quelle: Maulik et al 1998|
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|Tissue such as the myocardium can be adapted to ischemic stress by repeatedly subjecting it to short terms of reversible ischemia, each followed by another short duration of reperfusion108, 109. This phenomenon causes the production of oxidative stress, leading to the induction of gene expression, which is subsequently translated into the development of beneficial proteins responsible for the heart’s defence97.
97. Murphy E, Steenbergen C. Mechanisms Underlying Acute Protection From Cardiac Ischemia-Reperfusion Injury. Physiol. Rev. 2008;88:581-609.
108. Maulik N, Yoshida T, Zu YL, Sato M, Banerjee A, Das DK. Ischemic preconditioning triggers tyrosine kinase signaling: a potential role for MAPKAP kinase 2. Am J Physiol. 1998;275:H1857-1864.
109. Maulik N, Yoshida T, Engelman RM, Deaton D, Flack JE, 3rd, Rousou JA, Das DK. Ischemic preconditioning attenuates apoptotic cell death associated with ischemia/reperfusion. Mol Cell Biochem. 1998;186:139-145.
|Mammalian heart can be adapted to ischemia by repeatedly subjecting it to short-term reversible ischemia each followed by another short duration of reperfusion [1,2]. This phenomenon, known as ischemic adaptation, causes the production of oxidative stress leading to the induction of gene expression which is subsequently translated into the development of several stress-related proteins responsible for the heart's defense .
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