Diabetes represents a group of heterogenous metabolic diseases which share the appearance of hyperglycemia. In this context, activation of the mammalian target of rapamycin (mTOR) is a double-edge sword for the regulation of ß cell mass and function, and consequently, for diabetes development. Furthermore, mTOR signaling regulates multiple biological process and it is a negative regulator of autophagy. Autophagy is a cellular degradation and recycling process highly conserved in all eukaryotes that plays an important role in maintaining cellular homeostasis in response to intracellular stress by removing misfolded or aggregated proteins, as well as eliminating intracellular pathogens. It has been largely demonstrated that a chronic hyperactivation of mTOR signaling and/or dysfunction in autophagy leads to beta-cell dysfunction and the progression of diabetes.
The main goal of this research topic is focused on study different biological processes and molecular mechanisms regulating beta cell homeostasis. Specifically, our interests are to deepen into:
1. The posttranslational modifications of different proteins involved in metabolism.
2. The molecular mechanisms governing mTORC1 activity to identify new compounds to treat diabetes
3. The search for new modulators of autophagic and mitophagic processes that could reduce oxidative and ER stress
4. Signaling pathways altered during the progression to the disease (mainly in T1DM and T2DM)
5. Cellular mechanisms which could explain the progression of the disease
6. Metabolic and epigenetic changes occurring during the progression of diabetes (T1DM and T2DM)
Both research papers and review manuscripts are welcomed.
Diabetes represents a group of heterogenous metabolic diseases which share the appearance of hyperglycemia. In this context, activation of the mammalian target of rapamycin (mTOR) is a double-edge sword for the regulation of ß cell mass and function, and consequently, for diabetes development. Furthermore, mTOR signaling regulates multiple biological process and it is a negative regulator of autophagy. Autophagy is a cellular degradation and recycling process highly conserved in all eukaryotes that plays an important role in maintaining cellular homeostasis in response to intracellular stress by removing misfolded or aggregated proteins, as well as eliminating intracellular pathogens. It has been largely demonstrated that a chronic hyperactivation of mTOR signaling and/or dysfunction in autophagy leads to beta-cell dysfunction and the progression of diabetes.
The main goal of this research topic is focused on study different biological processes and molecular mechanisms regulating beta cell homeostasis. Specifically, our interests are to deepen into:
1. The posttranslational modifications of different proteins involved in metabolism.
2. The molecular mechanisms governing mTORC1 activity to identify new compounds to treat diabetes
3. The search for new modulators of autophagic and mitophagic processes that could reduce oxidative and ER stress
4. Signaling pathways altered during the progression to the disease (mainly in T1DM and T2DM)
5. Cellular mechanisms which could explain the progression of the disease
6. Metabolic and epigenetic changes occurring during the progression of diabetes (T1DM and T2DM)
Both research papers and review manuscripts are welcomed.
