Open AccessPathophysiological Consequences of TAT-HKII Peptide Administration Are Independent of Impaired Vascular Function and Ensuing Ischemia
Author(s) -
Rianne Nederlof,
Chaoqin Xie,
Otto Eerbeek,
Anneke Koeman,
Dan M.J. Milstein,
Markus W. Hollmann,
Egbert G. Mik,
Alice Warley,
Richard Southworth,
Fadi G. Akar,
Coert J. Zuurbier
Publication year - 2013
Publication title -
circulation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.899
H-Index - 336
eISSN - 1524-4571
pISSN - 0009-7330
DOI - 10.1161/circresaha.112.274308
Subject(s) - ischemia , cardioprotection , ischemic preconditioning , cardiac function curve , mitochondrion , medicine , pharmacology , endocrinology , microbiology and biotechnology , biology , heart failure
We have shown that partial dissociation of hexokinase II (HKII) from mitochondria in the intact heart using low-dose transactivating transcriptional factor (TAT)-HKII (200 nmol/L) prevents the cardioprotective effects of ischemic preconditioning, whereas high-dose TAT-HKII (10 μmol/L) administration results in rapid myocardial dysfunction, mitochondrial depolarization, and disintegration. In this issue of Circulation Research, Pasdois et al argue that the deleterious effects of TAT-HKII administration on cardiac function are likely because of vasoconstriction and ensuing ischemia.
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