Programmed cell death (PCD) is a cell-autonomous process regulated by distinct molecular mechanisms. Recently, many new types of PCD, called non-apoptotic programmed cell death (NAPCD), have been identified. These include ferroptosis, pyroptosis, cuproptosis, autophagy, necroptosis, entosis immunogenic cell death, and anoikis. Emerging evidence indicates that NAPCD is involved in the pathogenesis of human diseases including cardiovascular, neurological disorders and cancers, and thus a better understanding of the NAPCD will provide novel insights into pathophysiology, diagnosis and treatment. Although NAPCD, which is triggered by diverse extracellular and intracellular stresses, can cause tissue injuries and serious health problems, it kills cells by mechanisms different from apoptosis. Thus, NAPCD may be utilized to antagonize cancer growth, particularly chemo- and radio-resistant cancers.
A growing number of studies in recent years have uncovered many NAPCD-associated genes. These studies delved into changes in their expression as a mechanism. There are heritable changes that regulate gene expression, called epigenetics. These are not due to alterations in the sequence of DNA but caused by modifications, such as DNA methylation, histone modifications, RNAs modifications, non-coding RNAs, and chromatin remodeling, that exist in cells undergoing NAPCD. Utilizing the-state-of-the-art technologies, further investigations in this field will provide new opportunities in our understanding of the causal relationship between epigenetic modifications in NAPCD and the progression of human disease conditions. These studies may also provide the opportunity to identify key regulators in NAPCD, thereby serving as targets for novel therapeutic interventions.
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. Original research articles, methods, reviews, and mini-reviews are welcome. Specific areas of interest for the topic include but are not limited to the following:
1. Roles of epigenetic modification in non-apoptotic programmed cell death, including ferroptosis, pyroptosis, cuproptosis, autophagy, necroptosis, entosis, etc.
2. The molecular mechanisms driving epigenetic modification alterations in non-apoptotic programmed cell death.
3. Epigenetic modification and human diseases.
4. Diagnostic and prognostic potential of epigenetic modifications features in human diseases.
5. 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.
Programmed cell death (PCD) is a cell-autonomous process regulated by distinct molecular mechanisms. Recently, many new types of PCD, called non-apoptotic programmed cell death (NAPCD), have been identified. These include ferroptosis, pyroptosis, cuproptosis, autophagy, necroptosis, entosis immunogenic cell death, and anoikis. Emerging evidence indicates that NAPCD is involved in the pathogenesis of human diseases including cardiovascular, neurological disorders and cancers, and thus a better understanding of the NAPCD will provide novel insights into pathophysiology, diagnosis and treatment. Although NAPCD, which is triggered by diverse extracellular and intracellular stresses, can cause tissue injuries and serious health problems, it kills cells by mechanisms different from apoptosis. Thus, NAPCD may be utilized to antagonize cancer growth, particularly chemo- and radio-resistant cancers.
A growing number of studies in recent years have uncovered many NAPCD-associated genes. These studies delved into changes in their expression as a mechanism. There are heritable changes that regulate gene expression, called epigenetics. These are not due to alterations in the sequence of DNA but caused by modifications, such as DNA methylation, histone modifications, RNAs modifications, non-coding RNAs, and chromatin remodeling, that exist in cells undergoing NAPCD. Utilizing the-state-of-the-art technologies, further investigations in this field will provide new opportunities in our understanding of the causal relationship between epigenetic modifications in NAPCD and the progression of human disease conditions. These studies may also provide the opportunity to identify key regulators in NAPCD, thereby serving as targets for novel therapeutic interventions.
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. Original research articles, methods, reviews, and mini-reviews are welcome. Specific areas of interest for the topic include but are not limited to the following:
1. Roles of epigenetic modification in non-apoptotic programmed cell death, including ferroptosis, pyroptosis, cuproptosis, autophagy, necroptosis, entosis, etc.
2. The molecular mechanisms driving epigenetic modification alterations in non-apoptotic programmed cell death.
3. Epigenetic modification and human diseases.
4. Diagnostic and prognostic potential of epigenetic modifications features in human diseases.
5. 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.