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.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s10495-023-01905-6 | DOI Listing |
Sci Rep
January 2025
Emergency department, The Fourth Hospital of Hebei Medical University, Shijiazhuang, 050011, Hebei, China.
Esophageal squamous cell carcinoma (ESCC) is one of the most common digestive malignancies. Our previous studies revealed necroptosis-related lncRNA ENSG00000253385.1 was an independent prognostic factor for ESCC.
View Article and Find Full Text PDFChin Med J Pulm Crit Care Med
December 2024
Medical Research Center; The Zhejiang Key Laboratory of Intelligent Cancer, Biomarker Discovery and Translation, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, China.
Background: Necroptosis is a form of programmed cell death resulting in tissue inflammation due to the release of intracellular contents. Its role and regulatory mechanism in the context of acute lung injury (ALI) are unclear. Parkin (Prkn), an E3 ubiquitin ligase, has recently been implicated in the regulation of necroptosis.
View Article and Find Full Text PDFExp Eye Res
January 2025
Department of Ophthalmology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China. Electronic address:
The abrupt and substantial elevation of intraocular pressure (IOP) in acute glaucoma induces retinal ischemia/reperfusion (I/R) injury, resulting in progressive retinal ganglion cell (RGC) death and irreversible visual impairment. PANoptosis, a form of regulated cell death consisting of pyroptosis, apoptosis and necroptosis, is reported to be involved in high IOP-induced RGC death. However, the precise mechanisms of RGC death remain unclear, and neuroinflammation is considered to play a vital role.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Department of Thyroid and Breast Surgery, Ganzhou People's Hospital, 16 Meiguan Avenue, Ganzhou, Jiangxi Province 341000, PR China. Electronic address:
Sepsis associated acute lung injury (SALI) is a common complication in patients with severe sepsis and a disease with high morbidity and mortality in ICU patients. The main mechanism of SALI is pulmonary hypoperfusion due to hypotension and shock caused by sepsis, which leads to ischemic necrosis of alveolar endothelial cells and eventually lung failure. At present, SALI therapy mainly includes antibiotic therapy, fluid resuscitation, transfusion products and vasoactive drugs, but these strategies are not satisfactory.
View Article and Find Full Text PDFFEBS J
January 2025
Department of Biochemistry and Molecular Biology, School of Medicine, Southeast University, Nanjing, China.
TNFAIP3-interacting protein 1 (TNIP1; also known as ABIN-1) is a ubiquitin-binding protein that suppresses death-receptor- or Toll-like receptor-mediated apoptosis and necroptosis; however, it remains unclear whether ABIN-1 is capable of regulating pyroptosis. In the present study, we found that, in mouse embryonic fibroblasts and macrophages, ABIN-1 deficiency sensitized cells to poly(I:C) + TAK1 inhibitor 5Z-7-oxozeaenol-induced pyroptosis besides apoptosis and necroptosis. The sensitizing effect of ABIN-1 deficiency on pyroptosis depended on caspase-8 and its adaptor molecule FAS-associated death domain protein.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!