Augmented O-GlcNAc signaling attenuates oxidative stress and calcium overload in cardiomyocytes-Reference-Cited by-同舟云学术

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Augmented O-GlcNAc signaling attenuates oxidative stress and calcium overload in cardiomyocytes

Published:2010-08-27 Issue:3 Volume:40 Page:895-911
ISSN:0939-4451
Container-title:Amino Acids
language:en
Short-container-title:Amino Acids

Author:

Ngoh Gladys A.,Watson Lewis J.,Facundo Heberty T.,Jones Steven P.

Publisher

Springer Science and Business Media LLC

Subject

Organic Chemistry,Clinical Biochemistry,Biochemistry

Link

http://link.springer.com/content/pdf/10.1007/s00726-010-0728-7.pdf

Reference66 articles.

1. Akao M, Ohler A, O’Rourke B, Marban E (2001) Mitochondrial ATP-sensitive potassium channels inhibit apoptosis induced by oxidative stress in cardiac cells. Circ Res 88:1267–1275

2. Ambrosio G, Becker LC, Hutchins GM, Weisman HF, Weisfeldt ML (1986) Reduction in experimental infarct size by recombinant human superoxide dismutase: insights into the pathophysiology of reperfusion injury. Circulation 74:1424–1433

3. Bernardi P, Scorrano L, Colonna R, Petronilli V, Di Lisa F (1999) Mitochondria and cell death. Mechanistic aspects and methodological issues. Eur J Biochem 264:687–701

4. Bueno OF, De Windt LJ, Tymitz KM, Witt SA, Kimball TR, Klevitsky R, Hewett TE, Jones SP, Lefer DJ, Peng CF, Kitsis RN, Molkentin JD (2000) The MEK1-ERK1/2 signaling pathway promotes compensated cardiac hypertrophy in transgenic mice. EMBO J 19:6341–6350

5. Champattanachai V, Marchase RB, Chatham JC (2007) Glucosamine protects neonatal cardiomyocytes from ischemia–reperfusion injury via increased protein-associated O-GLcNAc. Am J Physiol Cell Physiol 292:C178–C187

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