About this Research Topic
Programmed cell death (PCD) is a crucial biological process that ensures the removal of damaged or unnecessary cells, maintaining cellular homeostasis. Traditionally, apoptosis has been the most studied form of PCD, but recent discoveries have identified various non-apoptotic programmed cell death (NAPCD) pathways, such as ferroptosis, pyroptosis, cuproptosis, autophagy, necroptosis, entosis, immunogenic cell death, and anoikis. These pathways are implicated in the pathogenesis of numerous human diseases, including cardiovascular and neurological disorders, as well as cancers. Unlike apoptosis, NAPCD is triggered by diverse stresses and can lead to tissue injuries, yet it also holds potential for combating cancer, especially in cases resistant to conventional therapies. Recent studies have highlighted the role of NAPCD-associated genes and their expression changes, driven by epigenetic modifications. These modifications, which include DNA methylation, histone modifications, RNA modifications, non-coding RNAs, and chromatin remodeling, do not alter the DNA sequence but significantly impact gene expression. Despite advancements, the intricate relationship between epigenetic modifications in NAPCD and disease progression remains underexplored, necessitating further research to uncover potential therapeutic targets.
This research topic aims to provide novel insights into the roles and mechanisms of epigenetic modifications in non-apoptotic programmed cell death related to human diseases. By exploring these mechanisms, the research seeks to elucidate the causal relationships between epigenetic changes and disease progression, offering potential pathways for diagnosis and treatment. The research will focus on understanding how these modifications influence NAPCD and identifying key regulators that could serve as targets for innovative therapeutic interventions.
To gather further insights in the realm of epigenetic modifications in NAPCD, we welcome articles addressing, but not limited to, the following themes:
- Roles of epigenetic modification in non-apoptotic programmed cell death, including ferroptosis, pyroptosis, cuproptosis, autophagy, necroptosis, entosis, etc.
- The molecular mechanisms driving epigenetic modification alterations in non-apoptotic programmed cell death.
- Epigenetic modification and human diseases.
- Diagnostic and prognostic potential of epigenetic modifications features in human diseases.
- Targeting epigenetic modifications as novel approaches for drug development.
This research topic aims to provide novel insights into the roles and mechanisms of epigenetic modifications in non-apoptotic programmed cell death related to human diseases. By exploring these mechanisms, the research seeks to elucidate the causal relationships between epigenetic changes and disease progression, offering potential pathways for diagnosis and treatment. The research will focus on understanding how these modifications influence NAPCD and identifying key regulators that could serve as targets for innovative therapeutic interventions.
To gather further insights in the realm of epigenetic modifications in NAPCD, we welcome articles addressing, but not limited to, the following themes:
- Roles of epigenetic modification in non-apoptotic programmed cell death, including ferroptosis, pyroptosis, cuproptosis, autophagy, necroptosis, entosis, etc.
- The molecular mechanisms driving epigenetic modification alterations in non-apoptotic programmed cell death.
- Epigenetic modification and human diseases.
- Diagnostic and prognostic potential of epigenetic modifications features in human diseases.
- Targeting epigenetic modifications as novel approaches for drug development.
Keywords: Non-apoptotic programmed cell death, epigenetic modification, gene expression, drug development, human diseases
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.
