About this Research Topic
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.
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