Mitochondria are the powerhouse of the cell, which produce most of the ATP to support cellular functions. In addition to their core metabolic roles, they also participate in regulation of multiple cellular processes, including calcium homeostasis, oxidative stress response, and apoptosis. Mitochondria are highly sensitive to environmental changes, such as nutrient restrictions, calcium overload, oxidative stress. Any disturbance in mitochondrial functions can alter cellular function and play a significant role in cell fate. For example, damaged mitochondria may lead to enhancement of ROS production, decrease of ATP production, Ca2+ overload, and triggering of cell death.
Due to their crucial role in modulation of cell functions, mitochondria have emerged as an important pharmacological target for the treatment of different diseases, such as cancer, heart failure, and neurodegenerative diseases, among others. However, the molecular mechanisms underlying mitochondria’s involvement in signaling and regulation of cell fate needs to be further elucidated. Mitochondrial homeostasis is maintained by a controlled balance between mitochondrial biogenesis and mitophagy and a tightly regulated interplay between external stimulations, including nutrients, calcium, oxidative stress, etc. A better understanding of the regulation mechanisms governing these processes is necessary to explore mitochondria-related diseases and their treatment. The aim of this Research Topic is to shed light on the molecular mechanisms underlying mitochondria’s involvement in control of cell fate, with particular focus on how defects in regulation of organelles’ signaling and function play a role in determination of cell fate and disease.
Topics of interest for this Research Topic include, but are not limited to:
• Mitochondrial homeostasis, signaling, disfunction and involvement in disease;
• mPTP and cell death (mitochondrial signaling pathway of apoptosis);
• Interplay between mitochondrial mitophagy and biogenesis;
• Cross talk between mitophagy and autophagy;
• Mitochondrial quality control and stem cell fate;
• Cross talk between mitochondrial ROS and calcium signaling;
• Nutrient induced mitochondrial dysfunction;
• Mitochondrial metabolism and cell function.
Mitochondria are the powerhouse of the cell, which produce most of the ATP to support cellular functions. In addition to their core metabolic roles, they also participate in regulation of multiple cellular processes, including calcium homeostasis, oxidative stress response, and apoptosis. Mitochondria are highly sensitive to environmental changes, such as nutrient restrictions, calcium overload, oxidative stress. Any disturbance in mitochondrial functions can alter cellular function and play a significant role in cell fate. For example, damaged mitochondria may lead to enhancement of ROS production, decrease of ATP production, Ca2+ overload, and triggering of cell death.
Due to their crucial role in modulation of cell functions, mitochondria have emerged as an important pharmacological target for the treatment of different diseases, such as cancer, heart failure, and neurodegenerative diseases, among others. However, the molecular mechanisms underlying mitochondria’s involvement in signaling and regulation of cell fate needs to be further elucidated. Mitochondrial homeostasis is maintained by a controlled balance between mitochondrial biogenesis and mitophagy and a tightly regulated interplay between external stimulations, including nutrients, calcium, oxidative stress, etc. A better understanding of the regulation mechanisms governing these processes is necessary to explore mitochondria-related diseases and their treatment. The aim of this Research Topic is to shed light on the molecular mechanisms underlying mitochondria’s involvement in control of cell fate, with particular focus on how defects in regulation of organelles’ signaling and function play a role in determination of cell fate and disease.
Topics of interest for this Research Topic include, but are not limited to:
• Mitochondrial homeostasis, signaling, disfunction and involvement in disease;
• mPTP and cell death (mitochondrial signaling pathway of apoptosis);
• Interplay between mitochondrial mitophagy and biogenesis;
• Cross talk between mitophagy and autophagy;
• Mitochondrial quality control and stem cell fate;
• Cross talk between mitochondrial ROS and calcium signaling;
• Nutrient induced mitochondrial dysfunction;
• Mitochondrial metabolism and cell function.
