About this Research Topic
Cell death is essential to maintain tissue homeostasis during normal development as well as to mount effective responses against pathogens. Apoptosis, pyroptosis, ferroptosis and necroptosis are the most investigated types of regulated cell death although new forms are continuously being reported. While apoptosis has been historically considered as a non-lytic, immunogenic silent type of cell death, ferroptosis, necroptosis and pyroptosis are characterized by the rupture of the cell membrane as a consequence of lipid peroxidation, or following the formation of gasdermin (GSDMs) or mixed lineage kinase domain-like pseudokinase (MLKL) pores, respectively. Lytic cell death causes the release of damage-associated molecular patterns (DAMPs) and has a strong impact on the surrounding milieu activating potent inflammatory reactions. In the context of bacterial infections, lytic cell death may also cause the escape of pathogens amplifying immune system activation. Despite being characterized by distinct molecular triggers, signalling axes and execution mechanisms, these pathways display extensive crosstalk.
Growing evidence suggests that dysregulation of cell death contributes to chronic inflammation and to the progression of acute conditions, such as infectious diseases. Therefore, fine-tuning of cell death is a promising strategy for treating inflammation in several contexts and a better understanding of its molecular mechanisms is of paramount importance for the development of more effective therapies.
The goal of this Research Topic is to explore novel molecular mechanisms leading to cell death and their contribution to inflammatory diseases. In this respect, both chronic and acute inflammatory conditions in sterile and infective settings will be investigated. We expect to discover new interactions among cell death pathways, as in the case of caspase-8: originally classified as purely apoptotic enzyme, caspase-8 is now recognized to be central in several types of cell death as it promotes pyroptosis directly, through cleavage of GSDMD and GSDMC, or indirectly, through caspase-3-dependent cleavage of GSDME.
We expect to receive contributions addressing the proposed topic through highly different and complementary approaches, ranging from biophysics to cell and molecular biology up to preclinical studies.
In this Research Topic, we welcome the submission of Original Research, Methods, Brief Research Reports, and Review Articles covering, but not limited to, the following sub-topics:
• New insights on the mechanisms leading to inflammasome activation and pyroptosis.
• Molecular mechanisms of ferroptosis and necroptosis.
• Gasdermin activation and pore formations.
• Activation of caspases and their cross-talk.
• Role of lipids in the regulation of cell death.
• Impact of inflammatory cell death on chronic inflammatory diseases.
• Role of cell death in infectious diseases.
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this topic.
Growing evidence suggests that dysregulation of cell death contributes to chronic inflammation and to the progression of acute conditions, such as infectious diseases. Therefore, fine-tuning of cell death is a promising strategy for treating inflammation in several contexts and a better understanding of its molecular mechanisms is of paramount importance for the development of more effective therapies.
The goal of this Research Topic is to explore novel molecular mechanisms leading to cell death and their contribution to inflammatory diseases. In this respect, both chronic and acute inflammatory conditions in sterile and infective settings will be investigated. We expect to discover new interactions among cell death pathways, as in the case of caspase-8: originally classified as purely apoptotic enzyme, caspase-8 is now recognized to be central in several types of cell death as it promotes pyroptosis directly, through cleavage of GSDMD and GSDMC, or indirectly, through caspase-3-dependent cleavage of GSDME.
We expect to receive contributions addressing the proposed topic through highly different and complementary approaches, ranging from biophysics to cell and molecular biology up to preclinical studies.
In this Research Topic, we welcome the submission of Original Research, Methods, Brief Research Reports, and Review Articles covering, but not limited to, the following sub-topics:
• New insights on the mechanisms leading to inflammasome activation and pyroptosis.
• Molecular mechanisms of ferroptosis and necroptosis.
• Gasdermin activation and pore formations.
• Activation of caspases and their cross-talk.
• Role of lipids in the regulation of cell death.
• Impact of inflammatory cell death on chronic inflammatory diseases.
• Role of cell death in infectious diseases.
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this topic.
Keywords: Pyroptosis, necroptosis, apoptosis, cross-talk, inflammasome, gasdermin, pores, caspases, infectious disease, chronic inflammation, PAMPs, DAMPs
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
