The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.
Regulation of myocardial growth and death by NADPH oxidase
Open accessAbstract
The NADPH oxidases (Nox) are transmembrane proteins dedicated to producing reactive oxygen species (ROS), including superoxide and hydrogen peroxide, by transferring electrons from NAD(P)H to molecular oxygen. Nox2 and Nox4 are expressed in the heart and play an important role in mediating oxidative stress at baseline and under stress. Nox2 is primarily localized on the plasma membrane, whereas Nox4 is found primarily on intracellular membranes, on mitochondria, the endoplasmic reticulum or the nucleus. Although Nox2 plays an important role in mediating angiotensin II-induced cardiac hypertrophy, Nox4 mediates cardiac hypertrophy and heart failure in response to pressure overload. Expression of Nox4 is upregulated by hypertrophic stimuli, and Nox4 in mitochondria plays an essential role in mediating oxidative stress during pressure overload-induced cardiac hypertrophy. Upregulation of Nox4 induces oxidation of mitochondrial proteins, including aconitase, thereby causing mitochondrial dysfunction and myocardial cell death. On the other hand, Noxs also appear to mediate physiological functions, such as erythropoiesis and angiogenesis. In this review, we discuss the role of Noxs in mediating oxidative stress and both pathological and physiological functions of Noxs in the heart.
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Cites
The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology
Bedard, K., & Krause, K.-H. (2007) · Physiological Reviews · doi:10.1152/physrev.00044.2005 · Cited by 6,989
NOX enzymes and the biology of reactive oxygen
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Functional analysis of Nox4 reveals unique characteristics compared to other NADPH oxidases
Martyn, K. D., Frederick, L. M., von Loehneysen, K., Dinauer, M. C., & Knaus, U. G. (2006) · Cellular Signalling · doi:10.1016/j.cellsig.2005.03.023 · Cited by 783
NADPH oxidase 4 (Nox4) is a major source of oxidative stress in the failing heart
Kuroda, J., Ago, T., Matsushima, S., Zhai, P., Schneider, M. D., & Sadoshima, J. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1002178107 · Cited by 772
Self-citationA mechanistic role for cardiac myocyte apoptosis in heart failure
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NADPH Oxidases in Cardiovascular Health and Disease
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NOX4 activity is determined by mRNA levels and reveals a unique pattern of ROS generation
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“expressed in non-phagocytic cells in the heart, such as CMs and fibroblasts [9,12–22].”
Cited by
Mitochondrial Reactive Oxygen Species (ROS) and ROS-Induced ROS Release
Zorov, D. B., Juhaszova, M., & Sollott, S. J. (2014) · Physiological Reviews · doi:10.1152/physrev.00026.2013 · Cited by 5,383
ROS and redox signaling in myocardial ischemia-reperfusion injury and cardioprotection
Cadenas, S. (2018) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2018.01.024 · Cited by 820
Münzel, T., Gori, T., Keaney, J. F., Maack, C., & Daiber, A. (2015) · European Heart Journal · doi:10.1093/eurheartj/ehv305 · Cited by 394
Zhao, L., Tao, X., Qi, Y., Xu, L., Yin, L., & Peng, J. (2018) · Redox Biology · doi:10.1016/j.redox.2018.02.026 · Cited by 202
Matsushima, S., Kuroda, J., Ago, T., Zhai, P., Park, J. Y., Xie, L.-H., Tian, B., & Sadoshima, J. (2013) · Circulation Research · doi:10.1161/circresaha.112.279760 · Cited by 183
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Metadata
- Authors
- Maejima, Y., Kuroda, J., Matsushima, S., Ago, T., & Sadoshima, J.
- Venue
- Journal of Molecular and Cellular Cardiology
- Publisher
- Elsevier BV
- Published
- 2011-03
- Volume
- 50
- Issue
- 3
- Pages
- 408-416
- ISSN
- 0022-2828 (ISSN-L)
- OpenAlex
- W1983045014
- Cited by
- 184
- References
- 16
- FWCI
- 14.25
- Type
- journal article
- Language
- en
- Open access
- green
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