Autophagy is an evolutionarily conserved catabolic process that delivers cytoplasmic organelles and/or proteins to the lysosome for degradation. While autophagy was firstly found to promote cell survival in response to cellular stress by recycling the cellular components that supplies metabolic source, later studies revealed that overactivated autophagy can induce cell death by bulk degradation of intracellular organelles and cytosol, so that it is also referred to as “Type II programmed cell death”. Notably, the similar mechanisms that promote cell survival under some circumstances could induce cell death in others, in a manner with or without crosstalk of apoptosis, necrosis or ferroptosis. Therefore, the contribution of autophagy to cell death is highly context-dependent and remains a subject of active research in the field.
In this Research Topic, we aim to assemble recent advances in research on cell death induced by or related to autophagy. Specifically, we are trying to understand the mechanism that initiates lethal signaling and triggers autophagic cell death in both physiological and pathological conditions, including cell death induced by autophagy alone or incorporation with other types of cell death. In addition, we are also interested in the development of effective interventions targeting autophagy, such as the specific inhibition of autophagy without promoting apoptosis or resulting in irreversible loss of cellular functions. Along these lines, we wish to provide comprehensive insight into autophagy associated cell death, which could potentially develop autophagy related therapeutic targets in different diseases treatment.
All article types are welcome, including Original Research, Reviews, Mini reviews, Brief Research Reports, Perspective pieces, Hypothesis and Theory, Methods. Potential topics for submissions may include, but are not limited to:
• The molecules mechanisms that control autophagic cell death
• The role of autophagy related cell death in physiological process or disease models
• The crosstalk between autophagic cell death, apoptosis, necrosis, and ferroptosis
• Establishment of new strategies targeting autophagy related cell death
• Innovative approaches for monitoring cellular autophagic flux
We accept different article types. A full list of accepted article types, including descriptions, can be found at this link.
Keywords:
Cell death, autophagy, cellular degradation, autophagosome, lysosome
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.
Autophagy is an evolutionarily conserved catabolic process that delivers cytoplasmic organelles and/or proteins to the lysosome for degradation. While autophagy was firstly found to promote cell survival in response to cellular stress by recycling the cellular components that supplies metabolic source, later studies revealed that overactivated autophagy can induce cell death by bulk degradation of intracellular organelles and cytosol, so that it is also referred to as “Type II programmed cell death”. Notably, the similar mechanisms that promote cell survival under some circumstances could induce cell death in others, in a manner with or without crosstalk of apoptosis, necrosis or ferroptosis. Therefore, the contribution of autophagy to cell death is highly context-dependent and remains a subject of active research in the field.
In this Research Topic, we aim to assemble recent advances in research on cell death induced by or related to autophagy. Specifically, we are trying to understand the mechanism that initiates lethal signaling and triggers autophagic cell death in both physiological and pathological conditions, including cell death induced by autophagy alone or incorporation with other types of cell death. In addition, we are also interested in the development of effective interventions targeting autophagy, such as the specific inhibition of autophagy without promoting apoptosis or resulting in irreversible loss of cellular functions. Along these lines, we wish to provide comprehensive insight into autophagy associated cell death, which could potentially develop autophagy related therapeutic targets in different diseases treatment.
All article types are welcome, including Original Research, Reviews, Mini reviews, Brief Research Reports, Perspective pieces, Hypothesis and Theory, Methods. Potential topics for submissions may include, but are not limited to:
• The molecules mechanisms that control autophagic cell death
• The role of autophagy related cell death in physiological process or disease models
• The crosstalk between autophagic cell death, apoptosis, necrosis, and ferroptosis
• Establishment of new strategies targeting autophagy related cell death
• Innovative approaches for monitoring cellular autophagic flux
We accept different article types. A full list of accepted article types, including descriptions, can be found at this
link.
Keywords:
Cell death, autophagy, cellular degradation, autophagosome, lysosome
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.