1. Academic Validation
  2. Necroptosis inhibitors: mechanisms of action and therapeutic potential

Necroptosis inhibitors: mechanisms of action and therapeutic potential

  • Apoptosis. 2024 Feb;29(1-2):22-44. doi: 10.1007/s10495-023-01905-6.
Yingbo Zhou 1 Zhangtao Cai 1 Yijia Zhai 1 Jintao Yu 1 Qiujing He 2 Yuan He 3 Siriporn Jitkaew 4 Zhenyu Cai 5 6
Affiliations

Affiliations

  • 1 School of Medicine, Tongji University, Shanghai, 200092, China.
  • 2 School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China.
  • 3 Tongji University Cancer Center, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
  • 4 Center of Excellence for Cancer and Inflammation, Department of Clinical Chemistry, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok, 10330, Thailand.
  • 5 School of Medicine, Tongji University, Shanghai, 200092, China. [email protected].
  • 6 Tongji University Cancer Center, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, 200092, China. [email protected].
Abstract

Necroptosis is a type of programmed cell death that is morphologically similar to necrosis. This type of cell death is involved in various pathophysiological disorders, including inflammatory, neurodegenerative, infectious, and malignant diseases. Receptor-interacting protein kinase 1 (RIPK1), RIPK3, and Mixed Lineage Kinase domain-like protein (MLKL) pseudokinase constitute the core components of the Necroptosis signaling pathway and are considered the most promising targets for therapeutic intervention. The discovery and characterization of Necroptosis inhibitors not only accelerate our understanding of the Necroptosis signaling pathway but also provide important drug candidates for the treatment of necroptosis-related diseases. Here, we will review recent research progress on Necroptosis inhibitors, mechanisms of action and their potential applications for disease treatment.

Keywords

Inhibitors; MLKL; Necroptosis; RIPK1; RIPK3.

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