Two prominent roles of mitochondria are the production of ATP and the generation of metabolites for the synthesis of macromolecules. Beyond these two crucial functions, many studies have added evidence to support the role of mitochondria as signaling organelles. Mitochondria regulate a wide variety of cellular functions including proliferation and differentiation. There are multiple ways mitochondria have evolved to communicate its fitness to the rest of the cell. Activation of AMPK under low energy conditions to activate catabolism or the release of reactive oxygen species (ROS) to activate the hypoxic response are well-known examples. In addition, the release of mitochondrial DNA promotes inflammation in certain contexts and TCA cycle metabolites are involved in controlling many aspects of health, including aging, and contribute to pathology by mediating posttranslational modifications.
Defects in mitochondrial functions have been shown to impact cancer cell proliferation, stem cells differentiation, and immune cells functions. Distinct functions of mitochondria are required for different biological outcomes. For example, while the TCA cycle is necessary to maintain chromatin modifications, the maintenance of a membrane potential is required for the generation of ROS. The signaling pathways activated or repressed upon changes in mitochondrial function are likely to be cell type-specific. While it is clear now that mitochondria play an essential role in determining cell fate and function, in many contexts the molecular details of how changes in mitochondrial function affect the expression of specific genes remains to be elucidated. The goal of this research topic is to advance in our understanding of the mechanisms by which mitochondrial-dependent signaling events including the release of ROS or TCA cycle metabolites impact cell functions. In addition, emerging evidence indicates that beyond cell-autonomous functions, mitochondrial function control physiology through non-cell-autonomous signaling. It will be of high interest to understand how defects in mitochondria in specific cell types drive changes at the organism level.
• We are interested in research mechanistically studying how changes in mitochondrial function affect different biological outcomes at the cellular level.
• Studies addressing whether and how changes in mitochondrial metabolism in certain cell types influence the overall organism homeostasis are of high interest.
• Research in cancer, stem cells, and immunometabolism is of high interest.
A full list of accepted article types, including descriptions, can be found at this
linkTwo prominent roles of mitochondria are the production of ATP and the generation of metabolites for the synthesis of macromolecules. Beyond these two crucial functions, many studies have added evidence to support the role of mitochondria as signaling organelles. Mitochondria regulate a wide variety of cellular functions including proliferation and differentiation. There are multiple ways mitochondria have evolved to communicate its fitness to the rest of the cell. Activation of AMPK under low energy conditions to activate catabolism or the release of reactive oxygen species (ROS) to activate the hypoxic response are well-known examples. In addition, the release of mitochondrial DNA promotes inflammation in certain contexts and TCA cycle metabolites are involved in controlling many aspects of health, including aging, and contribute to pathology by mediating posttranslational modifications.
Defects in mitochondrial functions have been shown to impact cancer cell proliferation, stem cells differentiation, and immune cells functions. Distinct functions of mitochondria are required for different biological outcomes. For example, while the TCA cycle is necessary to maintain chromatin modifications, the maintenance of a membrane potential is required for the generation of ROS. The signaling pathways activated or repressed upon changes in mitochondrial function are likely to be cell type-specific. While it is clear now that mitochondria play an essential role in determining cell fate and function, in many contexts the molecular details of how changes in mitochondrial function affect the expression of specific genes remains to be elucidated. The goal of this research topic is to advance in our understanding of the mechanisms by which mitochondrial-dependent signaling events including the release of ROS or TCA cycle metabolites impact cell functions. In addition, emerging evidence indicates that beyond cell-autonomous functions, mitochondrial function control physiology through non-cell-autonomous signaling. It will be of high interest to understand how defects in mitochondria in specific cell types drive changes at the organism level.
• We are interested in research mechanistically studying how changes in mitochondrial function affect different biological outcomes at the cellular level.
• Studies addressing whether and how changes in mitochondrial metabolism in certain cell types influence the overall organism homeostasis are of high interest.
• Research in cancer, stem cells, and immunometabolism is of high interest.
A full list of accepted article types, including descriptions, can be found at this
link