Aberrant levels of cell death has been implicated in various diseases (e.g. cardiovascular diseases, cancers, and neurodegenerative diseases), enabling its specific modality as an essential therapeutic target. Mitochondrion, a key organelle in the acitvation process of the calssical regulated cell death—apoptosis, has been shown to interplay with other forms of cell death including as necroptosis, pyroptosis and ferroptosis according to recent publications.
In necroptosis, ?RIPK3 activates the pyruvate dehydrogenase complex, which increases mitochondrial respiration and augments mitochondrial ROS consequently. This not merely initiates the feedforward of necrosome (RIPK1 and RIPK3) assembly but also boosts RIPK3 activity, leading to necroptotic cell death. In pyroptosis, ?active GSDMD permeabilizes the plasma membrane as well as mitochondrial outer membrane permeabilization (MOMP). Moreover, the mobilized inflammasome activity further facilitates MOMP via BH3-only protein BID, expedite pyroptotic cell death. In ferroptosis, ?beyond affecting GPX4, cysteine deprivation also enhances glutaminolysis, which augments the mitochondrial tricarboxylic acid cycle, enhances aerobic respiration, and finally increases mitochondria-derived ROS. As a consequence of these events, ferroptotic cell death is accelerated.
Given the important roles of mitochondria, therapeutically inhibition of mitochondrial-associated cell death may hold tremendous treatment potential across different diseases.
While the involvement of mitochondria and cell death have been identified in different diseases, how mitochondria regulate cell death, and what are the new roles of this interplay, as well as how to prevent mitochondrial-associated cell death therapeutically remain to be better understood.
This special collection aims to collect the latest research advances on mitochondria-associated regulated cell death including necroptosis, pyroptosis and ferroptosis, and their new position in pathological development of different diseases.
Potential topics for submissions include but are not limited to:
· Ferroptosis and its involvement in the development of disesases
· The interplay between ferroptosis and mitochondria: history, mechanisms, and implications of diseases
· Necroptosis and mitochondria: their interplays in diseases
· Pyroptosis, Inflammation and Mitochondria: past, present, and future
· Multiple involvements of mitochondria and cell death: their roles in disease
· Mitochondria and regulated cell death: implications in neurodegenerative diseases
· Ferroptosis and novel cancer therapy
Aberrant levels of cell death has been implicated in various diseases (e.g. cardiovascular diseases, cancers, and neurodegenerative diseases), enabling its specific modality as an essential therapeutic target. Mitochondrion, a key organelle in the acitvation process of the calssical regulated cell death—apoptosis, has been shown to interplay with other forms of cell death including as necroptosis, pyroptosis and ferroptosis according to recent publications.
In necroptosis, ?RIPK3 activates the pyruvate dehydrogenase complex, which increases mitochondrial respiration and augments mitochondrial ROS consequently. This not merely initiates the feedforward of necrosome (RIPK1 and RIPK3) assembly but also boosts RIPK3 activity, leading to necroptotic cell death. In pyroptosis, ?active GSDMD permeabilizes the plasma membrane as well as mitochondrial outer membrane permeabilization (MOMP). Moreover, the mobilized inflammasome activity further facilitates MOMP via BH3-only protein BID, expedite pyroptotic cell death. In ferroptosis, ?beyond affecting GPX4, cysteine deprivation also enhances glutaminolysis, which augments the mitochondrial tricarboxylic acid cycle, enhances aerobic respiration, and finally increases mitochondria-derived ROS. As a consequence of these events, ferroptotic cell death is accelerated.
Given the important roles of mitochondria, therapeutically inhibition of mitochondrial-associated cell death may hold tremendous treatment potential across different diseases.
While the involvement of mitochondria and cell death have been identified in different diseases, how mitochondria regulate cell death, and what are the new roles of this interplay, as well as how to prevent mitochondrial-associated cell death therapeutically remain to be better understood.
This special collection aims to collect the latest research advances on mitochondria-associated regulated cell death including necroptosis, pyroptosis and ferroptosis, and their new position in pathological development of different diseases.
Potential topics for submissions include but are not limited to:
· Ferroptosis and its involvement in the development of disesases
· The interplay between ferroptosis and mitochondria: history, mechanisms, and implications of diseases
· Necroptosis and mitochondria: their interplays in diseases
· Pyroptosis, Inflammation and Mitochondria: past, present, and future
· Multiple involvements of mitochondria and cell death: their roles in disease
· Mitochondria and regulated cell death: implications in neurodegenerative diseases
· Ferroptosis and novel cancer therapy