Control of cellular bioenergetics by cytosolic calcium
Prof. Franck Norbert Gellerich from Otto-von-Guericke University, Germany will the 11th World Congress on Targeting Mitochondria 2020 Congress which will be held as Virtual Congress in October 29-30, 2020.
Summary of the abstract: To understand the regulation of cellular energy metabolism, it is necessary to consider spatiotemporal fluxes of OXPHOS key metabolites (adenine nucleotides, creatine, creatine phosphate, oxidizable substrates, oxygen, Ca2+) through mitochondrial membranes and dynamic diffusion barriers. I would like to focus on two shuttles supplying the OXPHOS with ADP and with pyruvate as well as their regulation by cytosolic Ca2+ (Ca2+cyt).
Targeting Mitochondria 2020 Congress
October 29-30, 2020 - Virtual congress
www.mitochondria-site.com
Variety of non-coding RNA imported and encoded in mitochondria
A special session will be dedicated to Non-coding RNAs in Nuclear-Mitochondrial Crosstalk: Applications for RNA Medicine
The objective of this special session is to share the latest advances on the ncRNA diversity, molecular mechanisms and their impact on mitochondrial functions and nuclear-mitochondrial crosstalk.
Dr. Eric Barrey from University Paris-Saclay, INRAE, AgroParisTech, France will chair & introduce the session.
For more information about speakers and presentations, please follow this link.
Targeting Mitochondria 2020 Congress
October 29-30, 2020 - Virtual congress
www.mitochondria-site.com
FBXL4 Deficiency leads to increased clearance of Mitochondria
The Organizing Committee of Targeting Mitochondria 2020 Congress is honored to announce the participation of Prof. Nils-Göran Larsson from Karolinska Institutet, Sweden.
Prof. Larsson will give a talk entitled "FBXL4 Deficiency leads to increased clearance of Mitochondria" during the congress which will be held on October 29-30, 2020.
Summary of the Talk: Pathogenic mutations inFBXL4 lead to OXPHOS defects and mtDNA depletion associated with encephalopathy, developmental regression, epileptic seizures and other types of neurological deficits. Despite the frequent occurrence and severe consequences of FBXL4 mutations in humans, the function of the FBXL4 protein has remained poorly understood. We generated mice that lack FBXL4 and show that they recapitulate important aspects of the human disease, including mtDNA depletion. Using proteomic approaches, we found a general decrease of mitochondrial proteins accompanied by an increase in lysosomal proteins inFbxl4 knockout mice as well as in fibroblasts derived from patients with loss-of-functionFBXL4mutations. Unexpectedly, expression of nuclear genes encoding mitochondrial proteins and mitochondrial translation remained unaffected in the absence of FBXL4. We present data showing that the molecular phenotype instead is explained by increased autophagic removal of mitochondria, leading to a global decrease of cellular mitochondrial content. Treatment with the lysosomal inhibitor ammonium chloride rescues mitochondrial protein stability inFBXL4knockout human cells, consistent with the hypothesis that increased autophagy flux is an important pathophysiological event. Further studies are needed to explore the therapeutic potential of these findings, in particular, whether inhibition of autophagy may provide a strategy for treatment of affected patients.
Targeting Mitochondria 2020 Congress
October 29-30, 2020
www.targeting-mitochondria.com
Roles for mitochondrial dysfunction in Alzheimer’s disease
The Scientific Committee of Targeting Mitochondria 2020 Congress invited Prof. Benedict C. Albensi from Max Rady College of Medicine - University of Manitoba, Canada to present his research on "Roles for mitochondrial dysfunction in Alzheimer’s disease" during the Targeting Mitochondria 2020 Congress, which will be held on October 29-30, 2020.
According to Prof. Benedict C. Albensi: Alzheimer’s disease (AD) is thought to be associated with multiple factors, where the greatest risk factor for AD is aging. In addition, much research has focused on amyloid beta and tau pathology as causative factors in AD. However, new data involving brain metabolic activity, proposes that altered mitochondria are a major force behind the development of AD. Understanding mitochondrial dysfunction and targeting mitochondrial bioenergetics could be a novel treatment approach holding great promise for preventing or treating AD.
For more information about Targeting Mitochondria 2020: https://targeting-mitochondria.com
Mitochondrial Dysfunction in Autism is Distinct from Mitochondrial Disease
The Organizing Committee of Targeting Mitochondria 2020 is honored to announce the participation of Prof. Richard E. Frye from Phoenix Children's Hospital, USA.
During the congress, Prof. Frye will give a strategic talk entitled "Mitochondrial Dysfunction in Autism is Distinct from Mitochondrial Disease".
Summary of the talk: Several lines of evidence suggest that mitochondrial function is not normal in many individuals with Autism Spectrum Disorder. However, the patterns of abnormalities found are unlike those seen in classic mitochondrial disease and include unique changes in electron transport chain activity, fatty acid metabolism and regulation of oxidative stress. This talk presents data that suggest that these unique abnormalities are a product of long-term metaplasticity adaptations resulting from exposure to extrinsic or intrinsic physiological stressors such as environmental exposures, microbiome alterations, nutrient deficiencies and/or inflammatory events.
Targeting Mitochondria 2020 Congress
October 29-30, 2020 - Berlin, Germany
www.mitochondria-site.com
Down Syndrome: Role of hydrogen sulfide overproduction in the pathogenesis of mitochondrial dysfunction
The Organizing Committee of Targeting Mitochondria 2020 honored to welcome Prof. Csaba Szabo from the Université de Fribourg, Switzerland.
Prof. Szabo will give a talk entitled "Down Syndrome: Role of hydrogen sulfide overproduction in the pathogenesis of mitochondrial dysfunction" during the congress which will be held on October 29-30, 2020 in Berlin, Germany.
Summary of the talk: Cystathionine-β-synthase (CBS) is one of the key mammalian enzymes that is responsible for the biological production of the gaseous transmitter hydrogen sulfide (H2S). When H2S is overproduced, it can exert detrimental cellular effects, in part due to inhibition of mitochondrial Complex IV activity. An increased expression of CBS and the consequent overproduction of H2S is well documented in individuals with Down syndrome (DS). Two decades ago, it has been proposed that a toxic overproduction of H2S importantly contributes to the metabolic and neurological deficits associated with DS. However, until recently, this hypothesis has not yet been tested experimentally. The present talk will present recent data generated in human dermal fibroblasts showing that DS cells overproduce H2S, which, in turn, suppresses mitochondrial Complex IV activity and impairs mitochondrial oxygen consumption and ATP generation. Therapeutic CBS inhibition lifts the tonic (and reversible) suppression of Complex IV: this results in the improvement of mitochondrial function in DS cells.
Targeting Mitochondria 2020 Congress
October 29-30, 2020 - Berlin, Germany
www.mitochondria-site.com
Mitochondrial disease community registry (MDCR): Perspectives from patients and families, lessons learned from the data
Mrs. Sophia Zilber from Boston, USA will join the Targeting Mitchondria 2020 Congress and will give a presentation entitled "Mitochondrial disease community registry (MDCR): Perspectives from patients and families, lessons learned from the data".
Patient-populated registries are an important component of rare disease communities for many reasons, including their use as a tool for gathering opinions on specific topics. The Mitochondrial Disease Community Registry (MDCR) was launched in 2014 by United Mitochondrial Disease Foundation (UMDF) for this purpose as well as to identify and characterize mitochondrial disease patients from the patient perspective. This talk presents data collected over a four year period and provided by adult mitochondrial disease patients and caregivers of pediatric mitochondrial disease patients. Findings suggest the importance of clinician-patient communication, need for treatment and cure, the impact of the disease on the entire life of a person, and quality of life as top issues as described by patients, while also highlighting that patients are hopeful and optimistic. Additionally, data quality checks showed that more clear and simple questions and shorter more-targeted surveys are needed in order to get accurate and meaningful data for research.
Targeting Mitochondria 2020 Congress
October 29-30, 2020
www.targeting-mitochondria.com
The Cell-free respiratory Competent Mitochondria in Blood: Strategic Role and Application
Prof. Alain Thierry from Montpellier Cancer Research Institute, INSERM, France will join the Targeting Mitochondria 2020 Congress which will be organized virtually and give a major presentation entitled "The Cell-free respiratory Competent Mitochondria in Blood: Strategic Role and Application".
The researchers used previous findings which showed that the plasma of a healthy individual contains up to 50,000 times more mitochondrial DNA than nuclear DNA. They hypothesized that for it to be detectable and quantifiable in the blood in this manner, the mitochondrial DNA had to be protected by a structure of sufficient stability. In order to identify such a structure, plasma samples from around 100 individuals were analyzed.
This analysis revealed the presence in the blood circulation of highly stable structures containing whole mitochondrial genomes. Following examination of their size and density, as well as the integrity of their mitochondrial DNA, these structures observed using electron microscopy (up to 3.7 million per ml of plasma) were revealed to be intact and functional mitochondria.
Read the complete news here: A New Blood Component Revealed
Targeting Mitochondria 2020 Congress
October 29-30, 2020
www.targeting-mitochondria.com
