Necroptosis is the best-described form of programmed necrosis triggered by Death Receptors, Toll-Like Receptors and interferons and dependent on Receptor Interacting Protein Kinase 3 (RIPK3) and its substrate Mixed-Lineage Kinase Like protein (MLKL). In recent years, necroptosis has emerged as an essential regulator of tissue homeostasis, innate immunity and inflammation. Aberrant activation of necroptosis can result in major life-threatening tissue damage and inflammatory reactions. The increasing body of knowledge on the molecular and cellular mechanisms regulating necroptosis has unraveled numerous checkpoints controlling necroptosis and identified several potential pharmacological targets. Finally, more recently, identification of genetic mutations affecting the necroptotic pathway in patients has highlighted its importance in human diseases.
The aim of this article collection is to provide an up-to-date review of the role of necroptosis in tissue homeostasis, with a specific focus on its role in human diseases, while also encouraging the submission of new data. The Research Topic will discuss the function of necroptosis in host-pathogen interaction, tissue damage and inflammatory conditions as well as the potential therapeutic avenues of targeting necroptosis. This article collection will also address our current knowledge of the molecular regulation of necroptosis and necroptosis-dependent animal disease models. Finally, this Research Topic will also incorporate Original Research articles highlighting new and innovative research in the field.
The current issue will include both Review/Mini-Review and Original Research articles covering, but not limited to, the following aspects of necroptosis biology:
• Molecular and cellular regulation of necroptosis
• Necroptosis in host-pathogen interactions
• Necroptosis in animal models of tissue damage and inflammatory diseases.
• Necroptosis in human diseases
• Therapeutic approaches targeting necroptosis
Necroptosis is the best-described form of programmed necrosis triggered by Death Receptors, Toll-Like Receptors and interferons and dependent on Receptor Interacting Protein Kinase 3 (RIPK3) and its substrate Mixed-Lineage Kinase Like protein (MLKL). In recent years, necroptosis has emerged as an essential regulator of tissue homeostasis, innate immunity and inflammation. Aberrant activation of necroptosis can result in major life-threatening tissue damage and inflammatory reactions. The increasing body of knowledge on the molecular and cellular mechanisms regulating necroptosis has unraveled numerous checkpoints controlling necroptosis and identified several potential pharmacological targets. Finally, more recently, identification of genetic mutations affecting the necroptotic pathway in patients has highlighted its importance in human diseases.
The aim of this article collection is to provide an up-to-date review of the role of necroptosis in tissue homeostasis, with a specific focus on its role in human diseases, while also encouraging the submission of new data. The Research Topic will discuss the function of necroptosis in host-pathogen interaction, tissue damage and inflammatory conditions as well as the potential therapeutic avenues of targeting necroptosis. This article collection will also address our current knowledge of the molecular regulation of necroptosis and necroptosis-dependent animal disease models. Finally, this Research Topic will also incorporate Original Research articles highlighting new and innovative research in the field.
The current issue will include both Review/Mini-Review and Original Research articles covering, but not limited to, the following aspects of necroptosis biology:
• Molecular and cellular regulation of necroptosis
• Necroptosis in host-pathogen interactions
• Necroptosis in animal models of tissue damage and inflammatory diseases.
• Necroptosis in human diseases
• Therapeutic approaches targeting necroptosis
