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Inflammation
Erschienen in: Inflammation 1/2024

27.09.2023 | RESEARCH

Anti-Necroptotic Effects of Itaconate and its Derivatives

verfasst von: Si-tao Ni, Qing Li, Ying Chen, Fu-li Shi, Tak-sui Wong, Li-sha Yuan, Rong Xu, Ying-qing Gan, Na Lu, Ya-ping Li, Zhi-ya Zhou, Li-hui Xu, Xian-hui He, Bo Hu, Dong-yun Ouyang

Erschienen in: Inflammation | Ausgabe 1/2024

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Abstract

Itaconate is an unsaturated dicarboxylic acid that is derived from the decarboxylation of the Krebs cycle intermediate cis-aconitate and has been shown to exhibit anti-inflammatory and anti-bacterial/viral properties. But the mechanisms underlying itaconate’s anti-inflammatory activities are not fully understood. Necroptosis, a lytic form of regulated cell death (RCD), is mediated by receptor-interacting protein kinase 1 (RIPK1), RIPK3, and mixed lineage kinase domain-like protein (MLKL) signaling. It has been involved in the pathogenesis of organ injury in many inflammatory diseases. In this study, we aimed to explore whether itaconate and its derivatives can inhibit necroptosis in murine macrophages, a mouse MPC-5 cell line and a human HT-29 cell line in response to different necroptotic activators. Our results showed that itaconate and its derivatives dose-dependently inhibited necroptosis, among which dimethyl itaconate (DMI) was the most effective one. Mechanistically, itaconate and its derivatives inhibited necroptosis by suppressing the RIPK1/RIPK3/MLKL signaling and the oligomerization of MLKL. Furthermore, DMI promoted the nuclear translocation of Nrf2 that is a critical regulator of intracellular redox homeostasis, and reduced the levels of intracellular reactive oxygen species (ROS) and mitochondrial superoxide (mtROS) that were induced by necroptotic activators. Consistently, DMI prevented the loss of mitochondrial membrane potential induced by the necroptotic activators. In addition, DMI mitigated caerulein-induced acute pancreatitis in mice accompanied by reduced activation of the necroptotic signaling in vivo. Collectively, our study demonstrates that itaconate and its derivatives can inhibit necroptosis by suppressing the RIPK1/RIPK3/MLKL signaling, highlighting their potential applications for treating necroptosis-associated diseases.
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Metadaten
Titel
Anti-Necroptotic Effects of Itaconate and its Derivatives
verfasst von
Si-tao Ni
Qing Li
Ying Chen
Fu-li Shi
Tak-sui Wong
Li-sha Yuan
Rong Xu
Ying-qing Gan
Na Lu
Ya-ping Li
Zhi-ya Zhou
Li-hui Xu
Xian-hui He
Bo Hu
Dong-yun Ouyang
Publikationsdatum
27.09.2023
Verlag
Springer US
Erschienen in
Inflammation / Ausgabe 1/2024
Print ISSN: 0360-3997
Elektronische ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-023-01909-z

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