Key result
Hypoxia-induced activation of PKC isoforms is mediated through phospholipase C and tyrosine kinase pathways, whereas oxidative stress activates PKC independently of these pathways.
Population
Isolated adult guinea pig hearts perfused by the Langendorff method
Design
Preclinical
Authors
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No direct clinical translation yet; leaves open stimulus-specific PKC modulation in cardiac stress models.
Oxidative stress activates cardiac PKC isoforms independently of Galphaq-phospholipase C and tyrosine kinase signaling, highlighting distinct regulatory pathways for different pathological stimuli.
Takeishi et al. (1999) studied Myocardial ischemia and oxidative stress. Ischemia, hypoxia, H(2)O(2), or angiotensin II was evaluated on Translocation of PKC isoforms. Hypoxia-induced activation of PKC isoforms is mediated through phospholipase C and tyrosine kinase pathways, whereas oxidative stress activates PKC independently of these pathways.
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