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Activation of α1B-adrenoceptors contributes to intermittent hypobaric hypoxia-improved postischemic myocardial performance via inhibiting MMP-2 activation.

Am J Physiol Heart Circ Physiol

June 2014

Key Laboratory of Stem Cell Biology and Laboratory of Molecular Cardiology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine Shanghai, China; and

Article Synopsis
  • Intermittent hypobaric hypoxia (IHH) protects the heart from ischemia/reperfusion (I/R) injury by regulating the activation of matrix metalloproteinase-2 (MMP-2) and its related signaling pathways.
  • IHH enhances myocardial function and reduces damage (like infarct size and lactate dehydrogenase release) in isolated rat hearts following I/R injury.
  • The cardioprotection provided by IHH involves the modulation of α1-adrenoceptors, specifically increasing the density of α1A and α1B receptors, and activating the PKC epsilon pathway, which helps to manage MMP-2 activation and oxidative stress responses.
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