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Rapid Communication | Open Access

Neurokinin-2 receptor antagonist SR48968 induced necroptosis of myeloid leukemia cells by calcium overload-driven reactive oxygen species accumulation

Zhibin Yana,1Xiangyu Honga,1Qihao LinaLeijie WangbGang ShaoaChentao GeaRuilong XiaaCaiyun Fua( )
Zhejiang Provincial Key Laboratory of Silkworm Bioreactor and Biomedicine, College of Life Sciences and Medicine, Zhejiang Sci-Tech University, Hangzhou, Zhejiang 310018, China
College of Life Sciences, China Jiliang University, Hangzhou, Zhejiang 310018, China

1 These authors contributed equally to this work.

Peer review under responsibility of Chongqing Medical University.

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References

1

Ge C, Huang H, Huang F, et al. Neurokinin-1 receptor is an effective target for treating leukemia by inducing oxidative stress through mitochondrial calcium overload. Proc Natl Acad Sci U S A. 2019;116(39):19635–19645.

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Koschel J, Nishanth G, Just S, et al. OTUB1 prevents lethal hepatocyte necroptosis through stabilization of c-IAP1 during murine liver inflammation. Cell Death Differ. 2021;28(7):2257–2275.

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Vanden Berghe T, Vanlangenakker N, Parthoens E, et al. Necroptosis, necrosis and secondary necrosis converge on similar cellular disintegration features. Cell Death Differ. 2010;17(6):922–930.

4

Weindel CG, Martinez EL, Zhao X, et al. Mitochondrial ROS promotes susceptibility to infection via gasdermin D-mediated necroptosis. Cell. 2022;185(17):3214–3231.e23.

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Peng TI, Jou MJ. Oxidative stress caused by mitochondrial calcium overload. Ann N Y Acad Sci. 2010;1201:183–188.

Genes & Diseases
Article number: 101098
Cite this article:
Yan Z, Hong X, Lin Q, et al. Neurokinin-2 receptor antagonist SR48968 induced necroptosis of myeloid leukemia cells by calcium overload-driven reactive oxygen species accumulation. Genes & Diseases, 2024, 11(5): 101098. https://doi.org/10.1016/j.gendis.2023.101098

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Received: 19 February 2023
Published: 20 September 2023
© 2023 The Authors.

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

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