Macroautophagy (commonly, and hereafter in this text, referred to as autophagy) is a complex cellular process that plays a key role in the maintenance of cell homeostasis. It is positively modulated under conditions of nutrient deprivation and lack of energy in order to sustain cell survival by recycling cellular components. On the other hand, when nutrients are available, autophagy is inhibited. Either when autophagy is activated or inhibited, there is a crosstalk or a dynamic interplay with cell metabolism, thus, its function affects the cell metabolism and vice versa.
Autophagy acts by modulating several metabolic processes such as lipid, protein or carbohydrate metabolism. Many molecules are involved in the control of autophagy and its dialogue with metabolic control pathways. Among them, a key role is played by the mTORC complexes, AMPK and ULK1. It is becoming clear that these molecules (among others) may be considered as targets for the modulation of the autophagic process for therapeutic purposes.
Autophagy activity could be stimulated in those diseases characterized by an accumulation of protein aggregates in order to promote their removal or to remove damaged molecules and intracellular organelles, for example, to prevent cancer development or degenerative diseases. On the other hand, autophagy activity could be inhibited in those pathological conditions where this process exerts a promoting role, such as in cancer chemotherapy resistance, where the cells activate autophagy in order to acquire the capacity to withstand the damages exerted by chemotherapy agents and the hostile environment that establishes in the tumor periphery.
This Research Topic welcomes the contribution of papers (reviews, original research, perspectives) that can shed new light on the molecular mechanisms that regulate the interplay between autophagy and cell metabolism in physiological and pathological conditions and, in particular, on:
1) the mechanisms that modulate cell metabolism as a function of autophagy modulation, either in the presence or deficit of nutrients (such as selected amino acids or a mixture of several amino acids, glucose, etc);
2) small molecules that can pharmacologically modulate the autophagic process in physiological and pathological conditions;
3) the capacity of molecules normally present in food (or molecules that could be used in human nutrition) to modulate the autophagic process and the related metabolic pathways.
Macroautophagy (commonly, and hereafter in this text, referred to as autophagy) is a complex cellular process that plays a key role in the maintenance of cell homeostasis. It is positively modulated under conditions of nutrient deprivation and lack of energy in order to sustain cell survival by recycling cellular components. On the other hand, when nutrients are available, autophagy is inhibited. Either when autophagy is activated or inhibited, there is a crosstalk or a dynamic interplay with cell metabolism, thus, its function affects the cell metabolism and vice versa.
Autophagy acts by modulating several metabolic processes such as lipid, protein or carbohydrate metabolism. Many molecules are involved in the control of autophagy and its dialogue with metabolic control pathways. Among them, a key role is played by the mTORC complexes, AMPK and ULK1. It is becoming clear that these molecules (among others) may be considered as targets for the modulation of the autophagic process for therapeutic purposes.
Autophagy activity could be stimulated in those diseases characterized by an accumulation of protein aggregates in order to promote their removal or to remove damaged molecules and intracellular organelles, for example, to prevent cancer development or degenerative diseases. On the other hand, autophagy activity could be inhibited in those pathological conditions where this process exerts a promoting role, such as in cancer chemotherapy resistance, where the cells activate autophagy in order to acquire the capacity to withstand the damages exerted by chemotherapy agents and the hostile environment that establishes in the tumor periphery.
This Research Topic welcomes the contribution of papers (reviews, original research, perspectives) that can shed new light on the molecular mechanisms that regulate the interplay between autophagy and cell metabolism in physiological and pathological conditions and, in particular, on:
1) the mechanisms that modulate cell metabolism as a function of autophagy modulation, either in the presence or deficit of nutrients (such as selected amino acids or a mixture of several amino acids, glucose, etc);
2) small molecules that can pharmacologically modulate the autophagic process in physiological and pathological conditions;
3) the capacity of molecules normally present in food (or molecules that could be used in human nutrition) to modulate the autophagic process and the related metabolic pathways.
