Mitochondria, known as the "powerhouses of the cell", are a key feature of eukaryotic cells and generate the majority of cellular energy in the form of ATP. Uniquely, mitochondria have their own genome encoding essential components for the mitochondrial respiratory chain. They also communicate with the cell nucleus by receiving nuclear DNA-encoded proteins in an anterograde manner and/or sending ATP, Ca2+, ROS, and NAD+ to the nucleus by retrograde mitochondrial signaling. Aside from energy production and cell signaling, mitochondria are also involved in a wide range of other cellular processes, including quality control mechanisms, redox systems, cell proliferation, cell differentiation, cell senescence, cell death, genome instability, inflammation, and the immune response.
Due to the critical functions of mitochondria in the maintenance of cellular homeostasis, their dynamic nature which includes biogenesis, recycling through fusion and fission processes, and/or degradation via mitophagy, is pivotal for proper cellular and organismal physiology. In turn, mitochondrial dysfunction is a well-appreciated aging hallmark that is widely observed in aging, metabolic disorders, cancer, and neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, Friedreich ataxia, Lewy body disease, and spinal muscular atrophy.
Recent studies have identified novel concepts with which to probe the molecular mechanisms underlying mitochondrial biology, and considered how these may be harnessed for clinical applications. Promising mitochondria-targeted interventions await further investigation and development, including mitophagy stimulators like NAD+ precursors nicotinamide riboside and urolithin A, as well as mitochondria-based biomarker discovery, mitochondrial replacement therapy (MRT), and a novel method demonstrating the clinical potential of optogenetically manipulating mitochondria.
This Research Topic welcomes Original Research and Reviews articles on the current understanding and future perspectives of mitochondrial dysfunction in aging and neurodegenerative diseases, including underlying molecular and cellular mechanisms, methods to target and manipulate mitochondria, use of animal models, and the development of diagnostic or treatment tools, such as biomarkers for clinical practice. In particular, we welcome submissions on the following subtopics:
• Methodological approaches to target and manipulate the mitochondria.
• Phenotype and underlying molecular mechanisms of mitochondrial dysfunction in aging and neurodegenerative diseases.
• Use of animal models in the study of mitochondria function in aging and human diseases.
• Role of mitophagy in different brain cell types.
• Role of the mitochondria in DNA damage repair, cellular senescence, oxidative stress response, and redox signaling.
• Functions of the mitochondria in inflammation and immunity.
• Mitochondria-associated epigenetic regulation.
Mitochondria, known as the "powerhouses of the cell", are a key feature of eukaryotic cells and generate the majority of cellular energy in the form of ATP. Uniquely, mitochondria have their own genome encoding essential components for the mitochondrial respiratory chain. They also communicate with the cell nucleus by receiving nuclear DNA-encoded proteins in an anterograde manner and/or sending ATP, Ca2+, ROS, and NAD+ to the nucleus by retrograde mitochondrial signaling. Aside from energy production and cell signaling, mitochondria are also involved in a wide range of other cellular processes, including quality control mechanisms, redox systems, cell proliferation, cell differentiation, cell senescence, cell death, genome instability, inflammation, and the immune response.
Due to the critical functions of mitochondria in the maintenance of cellular homeostasis, their dynamic nature which includes biogenesis, recycling through fusion and fission processes, and/or degradation via mitophagy, is pivotal for proper cellular and organismal physiology. In turn, mitochondrial dysfunction is a well-appreciated aging hallmark that is widely observed in aging, metabolic disorders, cancer, and neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, Friedreich ataxia, Lewy body disease, and spinal muscular atrophy.
Recent studies have identified novel concepts with which to probe the molecular mechanisms underlying mitochondrial biology, and considered how these may be harnessed for clinical applications. Promising mitochondria-targeted interventions await further investigation and development, including mitophagy stimulators like NAD+ precursors nicotinamide riboside and urolithin A, as well as mitochondria-based biomarker discovery, mitochondrial replacement therapy (MRT), and a novel method demonstrating the clinical potential of optogenetically manipulating mitochondria.
This Research Topic welcomes Original Research and Reviews articles on the current understanding and future perspectives of mitochondrial dysfunction in aging and neurodegenerative diseases, including underlying molecular and cellular mechanisms, methods to target and manipulate mitochondria, use of animal models, and the development of diagnostic or treatment tools, such as biomarkers for clinical practice. In particular, we welcome submissions on the following subtopics:
• Methodological approaches to target and manipulate the mitochondria.
• Phenotype and underlying molecular mechanisms of mitochondrial dysfunction in aging and neurodegenerative diseases.
• Use of animal models in the study of mitochondria function in aging and human diseases.
• Role of mitophagy in different brain cell types.
• Role of the mitochondria in DNA damage repair, cellular senescence, oxidative stress response, and redox signaling.
• Functions of the mitochondria in inflammation and immunity.
• Mitochondria-associated epigenetic regulation.
