The aim of this Research Topic is to discuss recent developments in mitochondrial dysfunction. Mitochondrial dysfunction has developed as a factor underlying many neurological disorders and metabolic disorders, such as obesity, cancer, aging, hypertension, and type 2 diabetes (T2D). Mitochondrial aging leads to Endoplasmic Reticulum (ER) stress, fragmented mitochondria, ER stress-induced fragmented mitochondria, and altered cristae morphology. It has been long recognized that a deterioration in mitochondrial function causes pathophysiology and that this decline might contribute to the detected age-dependent decrease in organ function. Mitochondrial function across an individual’s life span is needed for general homeostasis. Mitochondria are an essential determinant of cellular fate by governing vital features, such as energy production and lipid biogenesis, or mediating the trigger of death programs. The endoplasmic reticulum and mitochondria continuously transfer information to sustain intracellular homeostasis. This transfer is achieved by physical contact between the two organelles. The physical contact of ER and mitochondria membranes creates a distinct microdomain termed either mitochondria-associated membranes (MAMs) or Mitochondrial Endoplasmic Reticulum Contact site (MERCs). Equally, MERCs dysfunction has been associated with Type 2 Diabetes, obesity, cardiovascular disease, and aging.
These specialized contact sites have been suggested to be enriched with specific proteins believed to be indispensable for mitochondrial calcium flux, lipid transfer, and morphology. Dysfunction of MERCs has been linked to skeletal muscle fat collection, which occurs during insulin resistance. Given the number of normal and pathological differences related to MERCs, there is a need for further studies of this relatively poorly understood structure and the mechanisms for how they impact disease conditions and how targeting them could lead to new protocols to treat these diseases. Therefore, in this research topic we will discuss the newest advances in techniques using transmission electron microscopy, 3D electron microscopy, super resolution techniques to identify organelle structure. We will also cover the most recent advances in the mitochondrial field, and lastly, showcase recent research articles on other organelle contact sites.
We have realized that there is a growing need for an integrative Research Topic that covers more holistic research around multiple disease states in the body that are caused by, or associated with, mitochondrial dysfunction.
In this Special Research Topic, we will cover the following themes in this collection:
• Insulin mediated structural changes in Mitochondria and MERCs
• Mitochondrial and MERC Metabolism
• Novel Regulators of Mitochondrial Metabolism (i.e., TMEM 135 and MICOS family of genes)
• Tissue Specific Age-related structural changes in Mitochondrial Function and MERC (i.e., heart, brain, and skeletal muscle).
• Disease related changes in Mitochondria Structure and MERC Structure
• Gap Junction related organelle contacts
• Methods on how to quantify mitochondria and MERCs.
Previous collections have focused on an interdisciplinary approach, but mostly on one organ. Here we aim to provide scientists and clinicians with a comprehensive, organ-based overview of human biology and disease pathophysiology from a clinical perspective. This will be comprehensive, covering all the major organ systems in the human body and how mitochondria and MERCs influence physiology and pathology. We also aim to use this Research Topic to educate scholars about the clinical setting rather than a fundamental science perspective alone.
The aim of this Research Topic is to discuss recent developments in mitochondrial dysfunction. Mitochondrial dysfunction has developed as a factor underlying many neurological disorders and metabolic disorders, such as obesity, cancer, aging, hypertension, and type 2 diabetes (T2D). Mitochondrial aging leads to Endoplasmic Reticulum (ER) stress, fragmented mitochondria, ER stress-induced fragmented mitochondria, and altered cristae morphology. It has been long recognized that a deterioration in mitochondrial function causes pathophysiology and that this decline might contribute to the detected age-dependent decrease in organ function. Mitochondrial function across an individual’s life span is needed for general homeostasis. Mitochondria are an essential determinant of cellular fate by governing vital features, such as energy production and lipid biogenesis, or mediating the trigger of death programs. The endoplasmic reticulum and mitochondria continuously transfer information to sustain intracellular homeostasis. This transfer is achieved by physical contact between the two organelles. The physical contact of ER and mitochondria membranes creates a distinct microdomain termed either mitochondria-associated membranes (MAMs) or Mitochondrial Endoplasmic Reticulum Contact site (MERCs). Equally, MERCs dysfunction has been associated with Type 2 Diabetes, obesity, cardiovascular disease, and aging.
These specialized contact sites have been suggested to be enriched with specific proteins believed to be indispensable for mitochondrial calcium flux, lipid transfer, and morphology. Dysfunction of MERCs has been linked to skeletal muscle fat collection, which occurs during insulin resistance. Given the number of normal and pathological differences related to MERCs, there is a need for further studies of this relatively poorly understood structure and the mechanisms for how they impact disease conditions and how targeting them could lead to new protocols to treat these diseases. Therefore, in this research topic we will discuss the newest advances in techniques using transmission electron microscopy, 3D electron microscopy, super resolution techniques to identify organelle structure. We will also cover the most recent advances in the mitochondrial field, and lastly, showcase recent research articles on other organelle contact sites.
We have realized that there is a growing need for an integrative Research Topic that covers more holistic research around multiple disease states in the body that are caused by, or associated with, mitochondrial dysfunction.
In this Special Research Topic, we will cover the following themes in this collection:
• Insulin mediated structural changes in Mitochondria and MERCs
• Mitochondrial and MERC Metabolism
• Novel Regulators of Mitochondrial Metabolism (i.e., TMEM 135 and MICOS family of genes)
• Tissue Specific Age-related structural changes in Mitochondrial Function and MERC (i.e., heart, brain, and skeletal muscle).
• Disease related changes in Mitochondria Structure and MERC Structure
• Gap Junction related organelle contacts
• Methods on how to quantify mitochondria and MERCs.
Previous collections have focused on an interdisciplinary approach, but mostly on one organ. Here we aim to provide scientists and clinicians with a comprehensive, organ-based overview of human biology and disease pathophysiology from a clinical perspective. This will be comprehensive, covering all the major organ systems in the human body and how mitochondria and MERCs influence physiology and pathology. We also aim to use this Research Topic to educate scholars about the clinical setting rather than a fundamental science perspective alone.