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NOX1, Reactive Oxygen Species, JNK, and Necrotic Cell Death

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Necrotic Cell Death

Part of the book series: Cell Death in Biology and Diseases ((CELLDEATH))

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Abstract

While programmed cell death with a necrotic phenotype has been studied for a number of years, until now many have dismissed the phenomenon as an in vitro artifact of tissue culture conditions. Due to recent in vivo studies suggesting that it is pertinent to mammalian development, programmed necrotic cell death can now be clearly classified as a bona fide classification of cell death. Among the original observations about programmed necrotic cell phenomenon was data suggesting that reactive oxygen species (ROS) played a substantial role in this form of cell death. This requirement for ROS continues to be validated in general in many current studies. ROS play many substantial roles in physiological and pathological signaling processes, as well as act as causative agents of cellular damage. There are many potential cellular sources of reactive oxygen species generation, including the NOX1 and other NADPH oxidases), the mitochondria, and other cytoplasmic enzymes. Although NADPH oxidases may contribute to ROS generation under necrotic conditions, the mitochondria are thought to play a significant role in necrotic cell death and may function as the initial source of ROS, the ROS amplification machinery, and a potential end target of ROS, leading to loss of mitochondrial function, with multiple consequences. The cellular sources of ROS likely feed on each other during the necrotic process, leading to a profound feed-forward amplification loop. As discussed, the stress-activated MAP kinase, JNK, plays a substantial, intertwining role with ROS in potentiation of necrotic cell death through a wide variety of mechanisms, many of which appear to be context specific and which may be both upstream and downstream of ROS.

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  1. Department of Pharmacology, University of Colorado School of Medicine, Anschutz Medical Campus, Mail Stop 8303, Research 1 South, 12801 E. 17th Avenue, Rm. L18-6110, Aurora, CO, 80045, USA

    Michael J. Morgan Ph.D.

  2. Department of Biochemistry, Ajou University School of Medicine, San 5, Wonchon-dong, Yeongtong-gu, Suwon, 443-749, South Korea

    You-Sun Kim

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  1. Michael J. Morgan Ph.D.
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Correspondence to Michael J. Morgan Ph.D. .

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  1. Department of Physiology, National University of Singapore Yong Loo Lin School of Medicine, Singapore, Singapore

    Han-Ming Shen

  2. Department of Biomedical Molecular Biology (UGent), VIB/University of Ghent Inflammation Research Center (VIB), Zwijnaarde, Belgium

    Peter Vandenabeele

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Morgan, M.J., Kim, YS. (2014). NOX1, Reactive Oxygen Species, JNK, and Necrotic Cell Death. In: Shen, HM., Vandenabeele, P. (eds) Necrotic Cell Death. Cell Death in Biology and Diseases. Humana Press, New York, NY. https://doi.org/10.1007/978-1-4614-8220-8_8

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