Imagine a future where a single injection could retune your body’s faltering orchestra, restoring harmony to tissues frayed by time or disease—a vision that...
As direct descendants of ancient bacteria, mitochondria have always been a little alien.
Now a study shows that mitochondria are possibly even stranger than we...
A multidisciplinary team of scientists led by the University of Helsinki reports that a progressive neurodegenerative disease can be triggered by a viral infection. The mechanism relates to mitochondrial roles in antiviral defense mechanisms.
The scientists report that a specific gene variant affecting the mitochondria disturbs cellular antiviral defense responses. The results implicate that viral infections can trigger and modify symptoms of neurological diseases in subjects carrying genetic sensitivity.
‘Leaky” mitochondria can drive harmful inflammation which is responsible for diseases like lupus and rheumatoid arthritis. Now recent research published in the journal Nature Cell Biology from the University of Virginia Health System suggests that scientists may be able to develop better treatments for those diseases and improve our ability to fight off viruses and even slow aging.
The rates of obesity have nearly tripled since 1975, this alarming shift has resulted in a worldwide epidemic. Most certainly lifestyle factors such as diet, nutrition, exercise, physical activity, and sedentary time play critical roles in both the development and progress of obesity, but scientists have to understand that obesity is also associated with intrinsic metabolic abnormalities.
The maintenance of a balanced lipid homeostasis is critical for our health. While consumption of excessive amounts of fatty foods contributes to metabolic diseases such as obesity and atherosclerosis, fat is an indispensable component of our diet. Digested lipids supply the body with essential building blocks and facilitate the absorption of important vitamins.
In a new study published in the journal Nature, a team of researchers led by Professor Manolis Pasparakis and their collaborators Professor Aleksandra Trifunovic and Professor Christian Frezza at the Excellence Cluster CECAD of the University of Cologne, and Professor Ju00f6rg Heeren at the University of Hamburg, report on a new mechanism that regulates the processing and transport of dietary lipids by the intestine.
A hungry cell has to be alerted to the presence of nutrients outside the cell wall by a sensing mechanism so a transporter protein can bring the nutrients inside. While only a handful have been identified, these nutrient-sensing mechanisms have a profound impact on health. However, within each cell, there are also self-contained, membrane-bound organelles that are equally in need of fuel to carry out important functions. Do they have nutrient sensors of their own?
Researchers have unveiled a new mechanism for regulating mitochondrial function. The findings reveal the critical role played by the enzymatic activity of the lysine acetyltransferase MOF in maintaining mitochondrial integrity and function through acetylation of mitochondrial electron transport chain component COX17. Cells lacking MOF-mediated COX17 acetylation exhibit dramatic mitochondrial defects and impaired ability to produce energy. Underscoring the clinical relevance of these findings, the team also showed that cells from human patients with a developmental disorder caused by mutations in MOF also exhibited respiratory defects that could be ameliorated by interventions such as acetylation-mimetic COX17 or mitochondrially targeted MOF.
Image: Electron microscopic image of neurons in the brain showing the presynaptic boutons (yellow), mitochondria (purple), and synapses (blue). Credit: Salk Institute
Salk scientists find mitochondria at dysfunctional synapses fail to meet energetic demand, supplying either too much or too little power and potentially causing age-related cognitive impairment
Microglia, a type of central nervous system cell, is primarily responsible for neuronal death in Leigh Syndrome and the neurological symptoms related to this mitochondrial disease. This is the conclusion of a research group from the Institut de Neurociu00e8ncies of the Universitat Autu00f2noma de Barcelona (INc-UAB) in a new study carried out on a mouse model of the disease. The study was coordinated by Juan Hidalgo, a researcher at the INc and the Department of Cell Biology, Physiology, and Immunology of the UAB, and published in the journal GLIA.
