The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Oxidative Stress Stimulates Autophagic Flux During Ischemia/Reperfusion
Open accessAbstract
Autophagy is a bulk degradation process in which cytosolic proteins and organelles are degraded through lysosomes. To evaluate autophagic flux in cardiac myocytes, we generated adenovirus and cardiac-specific transgenic mice harboring tandem fluorescent mRFP-GFP-LC3. Starvation significantly increased the number of mRFP-GFP-LC3 dots representing both autophagosomes and autolysosomes per cell, suggesting that autophagic flux is increased in cardiac myocytes. H(2)O(2) significantly increased autophagic flux, which was attenuated in the presence of N-2-mercaptopropionyl glycine (MPG), an antioxidant, suggesting that oxidative stress stimulates autophagy in cardiac myocytes. Myocardial ischemia/reperfusion (I/R) increased both autophagosomes and autolysosomes, thereby increasing autophagic flux. Treatment with MPG attenuated I/R-induced increases in oxidative stress, autophagic flux, and Beclin-1 expression, accompanied by a decrease in the size of myocardial infarction (MI)/area at risk (AAR), suggesting that oxidative stress plays an important role in mediating autophagy and myocardial injury during I/R. MI/AAR after I/R was significantly reduced in beclin1(+/-) mice, whereas beclin1(+/-) mice treated with MPG exhibited no additional reduction in the size of MI/AAR after I/R. These results suggest that oxidative stress plays an important role in mediating autophagy during I/R, and that activation of autophagy through oxidative stress mediates myocardial injury in response to I/R in the mouse heart.
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Cites
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Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes
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Self-citationReactive oxygen species are essential for autophagy and specifically regulate the activity of Atg4
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Response to myocardial ischemia/reperfusion injury involves Bnip3 and autophagy
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Cited by
Autophagy, mitochondria and oxidative stress: cross-talk and redox signalling.
Lee, J., Giordano, S., & Zhang, J. (2012) · Biochemical Journal · doi:10.1042/bj20111451 · Cited by 1,438
Cardioprotection and lifespan extension by the natural polyamine spermidine
Eisenberg, T., Abdellatif, M., Schroeder, S., Primessnig, U., Stekovic, S., Pendl, T., Harger, A., Schipke, J., Zimmermann, A., Schmidt, A., et al. (2016) · Nature Medicine · doi:10.1038/nm.4222 · Cited by 1,168
Self-citationMonitoring and Measuring Autophagy
Yoshii, S. R., & Mizushima, N. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18091865 · Cited by 1,107
Degradation of misfolded proteins in neurodegenerative diseases: Therapeutic targets and strategies
Ciechanover, A., & Kwon, Y. T. (2015) · Experimental & Molecular Medicine · doi:10.1038/emm.2014.117 · Cited by 898
ROS and Autophagy: Interactions and Molecular Regulatory Mechanisms
Li, L., Tan, J., Miao, Y., Lei, P., & Zhang, Q. (2015) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-015-0166-x · Cited by 876
Metadata
- Authors
- Hariharan, N., Zhai, P., & Sadoshima, J.
- Venue
- Antioxidants & Redox Signaling
- Publisher
- SAGE Publications
- Published
- 2011-06
- Volume
- 14
- Issue
- 11
- Pages
- 2179-2190
- ISSN
- 1523-0864 (ISSN-L)
- 1557-7716
- OpenAlex
- W2026660662
- Cited by
- 346
- References
- 8
- FWCI
- 11.53
- Type
- journal article
- Language
- en
- Open access
- green
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