Necroptosis inhibitors: mechanisms of action and therapeutic potential
- PMID: 38001341
- DOI: 10.1007/s10495-023-01905-6
Necroptosis inhibitors: mechanisms of action and therapeutic potential
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.
© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
Similar articles
-
The autophagy protein RUBCNL/PACER represses RIPK1 kinase-dependent apoptosis and necroptosis.Autophagy. 2024 Nov;20(11):2444-2459. doi: 10.1080/15548627.2024.2367923. Epub 2024 Jul 3. Autophagy. 2024. PMID: 38873940 Free PMC article.
-
Inhibition of RIPK1 or RIPK3 kinase activity post ischemia-reperfusion reduces the development of chronic kidney injury.Biochem J. 2025 Jan 22;482(2):73-86. doi: 10.1042/BCJ20240569. Biochem J. 2025. PMID: 39705008 Free PMC article.
-
Hepatocyte necroptosis is associated with liver damage in dairy cows with ketosis.J Dairy Sci. 2025 Aug;108(8):8844-8858. doi: 10.3168/jds.2025-26349. Epub 2025 Jun 11. J Dairy Sci. 2025. PMID: 40513868
-
Necroptosis in myocardial ischaemia-reperfusion injury: current update on mechanisms, therapeutic targets, and translational potential.Apoptosis. 2025 Jun;30(5-6):1216-1234. doi: 10.1007/s10495-025-02108-x. Epub 2025 Mar 27. Apoptosis. 2025. PMID: 40146485 Review.
-
Recent advances in the role of gasotransmitters in necroptosis.Apoptosis. 2025 Apr;30(3-4):616-635. doi: 10.1007/s10495-024-02057-x. Epub 2025 Jan 20. Apoptosis. 2025. PMID: 39833633 Review.
Cited by
-
Programmed Cell Death in Heart Failure: Mechanisms, Impacts, and Therapeutic Prospects.Rev Cardiovasc Med. 2025 Jul 28;26(7):38407. doi: 10.31083/RCM38407. eCollection 2025 Jul. Rev Cardiovasc Med. 2025. PMID: 40776946 Free PMC article. Review.
-
The molecular mechanisms, roles, and potential applications of PANoptosis in cancer treatment.Front Immunol. 2025 Apr 29;16:1550800. doi: 10.3389/fimmu.2025.1550800. eCollection 2025. Front Immunol. 2025. PMID: 40364845 Free PMC article. Review.
-
A cellular danse macabre: the choreography of programmed cell death.Apoptosis. 2025 Apr;30(3-4):507-511. doi: 10.1007/s10495-025-02076-2. Epub 2025 Feb 9. Apoptosis. 2025. PMID: 39924582
-
The relationship between immune cell infiltration and necroptosis gene expression in sepsis: an analysis using single-cell transcriptomic data.Front Cell Infect Microbiol. 2025 Aug 11;15:1618438. doi: 10.3389/fcimb.2025.1618438. eCollection 2025. Front Cell Infect Microbiol. 2025. PMID: 40861493 Free PMC article.
-
The interplay between α-synuclein aggregation and necroptosis in Parkinson's disease: a spatiotemporal perspective.Front Neurosci. 2025 Apr 8;19:1567445. doi: 10.3389/fnins.2025.1567445. eCollection 2025. Front Neurosci. 2025. PMID: 40264913 Free PMC article. Review.
References
Publication types
MeSH terms
Substances
Grants and funding
- X2022212/Tongji University Students Innovation Training Program
- 32170748/National Natural Science Foundation of China
- 21490714300/Shanghai Committee of Science and Technology
- 2022BFH02012/Key Research and Development Program of Ningxia
- 22120230107/Fundamental Research Funds for the Central Universities
LinkOut - more resources
Full Text Sources
Miscellaneous