Big data studies scrutinize links between fatty liver disease and how cells make energy
(American Society for Biochemistry and Molecular Biology) Three recent studies investigate changes in mitochondria, the cell's energy producers, as fatty liver disease (NAFLD) progresses to steatohepatosis (NASH). The first two studies illuminate how mitochondrial energy production stutters and fails; the third describes how changes to the liver during disease progression affect the organ's use of nutrients to produce energy. (Source: EurekAlert! - Medicine and Health)
Source: EurekAlert! - Medicine and Health - September 14, 2018 Category: International Medicine & Public Health Source Type: news

Changes in mitochondrial DNA control how nuclear DNA mutations are expressed in cardiomyopathy
(Children's Hospital of Philadelphia) Differences in the DNA within the mitochondria, the energy-producing structures within cells, can determine the severity and progression of heart disease caused by a nuclear DNA mutation. When combined with a mutation in nuclear DNA in animals, one mitochondrial DNA variant greatly worsened heart disease, while a different variant had a protective effect. (Source: EurekAlert! - Medicine and Health)
Source: EurekAlert! - Medicine and Health - September 11, 2018 Category: International Medicine & Public Health Source Type: news

Senior Research Laboratory Technician (Fixed Term)
We are looking for an experienced and enthusiastic individual to join the groups ofProfessor Abigail Fowden andDr Andrew Murray.Collectively, their research focuses on mitochondrial function during development and ageing, and how conditions during early life programme development can increase susceptibility to adult-onset degenerative diseases.The position is fixed-term, with funds available for 2 years in the first instance. The post holder will provide mainly molecular biology support, as well as some assistance with animal work, to ensure that the objectives of the research project are achieved.&nb...
Source: Society for Endocrinology - September 5, 2018 Category: Endocrinology Source Type: news

My Patient May Have a Mitochondrial Disease: What Should I Do? My Patient May Have a Mitochondrial Disease: What Should I Do?
All patients with a suspected mitochondrial disease should be seen by a mitochondrial medicine expert. But what can the primary care clinician do while waiting for that to happen?CHOP Expert Commentary (Source: Medscape Today Headlines)
Source: Medscape Today Headlines - August 17, 2018 Category: Consumer Health News Tags: Pediatrics Commentary Source Type: news

Frontiers in Metabolism meeting focuses on mechanisms of metabolic diseases
(Morgridge Institute for Research) A new scientific meeting hosted by the Morgridge Institute for Research will focus on the underlying mechanisms of metabolic diseases and innovations in the tools used to study them. The broad swath of topics will span cancer metabolism to lipid dysregulation to mitochondrial signaling. (Source: EurekAlert! - Medicine and Health)
Source: EurekAlert! - Medicine and Health - August 1, 2018 Category: International Medicine & Public Health Source Type: news

Heat therapy boosts mitochondrial function in muscles
(American Physiological Society) A new study finds that long-term heat therapy may increase mitochondrial function in the muscles. The discovery could lead to new treatments for people with chronic illness or disease. The study--the first of its kind in humans--is published ahead of print in the Journal of Applied Physiology. (Source: EurekAlert! - Social and Behavioral Science)
Source: EurekAlert! - Social and Behavioral Science - July 31, 2018 Category: International Medicine & Public Health Source Type: news

Mitochondrial redox sensing by the kinase ATM maintains cellular antioxidant capacity
Mitochondria are integral to cellular energy metabolism and ATP production and are involved in regulating many cellular processes. Mitochondria produce reactive oxygen species (ROS), which not only can damage cellular components but also participate in signal transduction. The kinase ATM, which is mutated in the neurodegenerative, autosomal recessive disease ataxia-telangiectasia (A-T), is a key player in the nuclear DNA damage response. However, ATM also performs a redox-sensing function mediated through formation of ROS-dependent disulfide-linked dimers. We found that mitochondria-derived hydrogen peroxide promoted ATM d...
Source: Signal Transduction Knowledge Environment - July 10, 2018 Category: Science Authors: Zhang, Y., Lee, J.-H., Paull, T. T., Gehrke, S., DAlessandro, A., Dou, Q., Gladyshev, V. N., Schroeder, E. A., Steyl, S. K., Christian, B. E., Shadel, G. S. Tags: STKE Research Articles Source Type: news

The association between cortisol, oxytocin, and immune cell mitochondrial oxygen consumption in postpartum women with childhood maltreatment - Boeck C, Gumpp AM, Calzia E, Radermacher P, Waller C, Karabatsiakis A, Kolassa IT.
Childhood maltreatment (CM) is associated with an increased risk for the development of psychiatric and somatic diseases in later life. Individual risk and resilience factors may, however, influence how deep psychological stress gets under the skin. We hyp... (Source: SafetyLit)
Source: SafetyLit - June 18, 2018 Category: International Medicine & Public Health Tags: Age: Adolescents Source Type: news

Mutation links bipolar disorder to mitochondrial disease
(RIKEN) Mutations in the gene ANT1 may confer a risk for bipolar disorder through a complex interplay between serotonin and mitochondrial signaling in the brain. These two pathways have been separately implicated in bipolar disorder, but the link between levels of the neurotransmitter serotonin and mitochondrial dysfunction had not been established. Researchers at the RIKEN Center for Brain Science (CBS) in Japan now report that mitochondrial dysfunction affects the activity of serotonergic neurons in mice with mutations of ANT1. (Source: EurekAlert! - Medicine and Health)
Source: EurekAlert! - Medicine and Health - June 11, 2018 Category: International Medicine & Public Health Source Type: news

What would help or hinder patient participation in mitochondrial disease clinical trials?
As clinical trials gear up with the aim of attaining the first FDA-approved treatments for mitochondrial disease, a new study reports for the first time what patients and families say would motivate them for or against participating in such research trials. Based in malfunctions in mitochondria, the tiny structures within cells that act as biological batteries, mitochondrial disease is a highly variable collection of energy deficiency disorders that can affect nearly any and all organs and systems - at any age. (Source: World Pharma News)
Source: World Pharma News - June 7, 2018 Category: Pharmaceuticals Tags: Featured Research Research and Development Source Type: news

Biomedical optics engineer Jesse Wilson named a Boettcher Investigator
(Colorado State University) Mitochondrial diseases are devastating illnesses caused by defects in cellular organelles called mitochondria. Their cells starved of energy, most stricken children die by age 12. There is no cure, and diagnosis can take months.Colorado State University biomedical engineer Jesse Wilson wants to change all of that. The assistant professor of electrical and computer engineering is proposing a radical new imaging technology that could diagnose mitochondrial defects in an instant. (Source: EurekAlert! - Medicine and Health)
Source: EurekAlert! - Medicine and Health - June 7, 2018 Category: International Medicine & Public Health Source Type: news

Mitochondrial Diseases: Current State of Understanding Mitochondrial Diseases: Current State of Understanding
Mitochondrial diseases can affect any system by causing any symptom in any organ by any mode of inheritance.CHOP Expert Commentary (Source: Medscape Today Headlines)
Source: Medscape Today Headlines - May 11, 2018 Category: Consumer Health News Tags: Pediatrics Commentary Source Type: news

MFN2 agonists reverse mitochondrial defects in preclinical models of Charcot-Marie-Tooth disease type 2A
Mitofusins (MFNs) promote fusion-mediated mitochondrial content exchange and subcellular trafficking. Mutations in Mfn2 cause neurodegenerative Charcot-Marie-Tooth disease type 2A (CMT2A). We showed that MFN2 activity can be determined by Met376 and His380 interactions with Asp725 and Leu727 and controlled by PINK1 kinase–mediated phosphorylation of adjacent MFN2 Ser378. Small-molecule mimics of the peptide-peptide interface of MFN2 disrupted this interaction, allosterically activating MFN2 and promoting mitochondrial fusion. These first-in-class mitofusin agonists overcame dominant mitochondrial defects provoked in ...
Source: ScienceNOW - April 19, 2018 Category: Science Authors: Rocha, A. G., Franco, A., Krezel, A. M., Rumsey, J. M., Alberti, J. M., Knight, W. C., Biris, N., Zacharioudakis, E., Janetka, J. W., Baloh, R. H., Kitsis, R. N., Mochly-Rosen, D., Townsend, R. R., Gavathiotis, E., Dorn, G. W. Tags: Cell Biology, Medicine, Diseases reports Source Type: news

Poor muscle health a complication of type 1 diabetes
Even active young adults with the disease have mitochondrial changes linked to cell damage Related items fromOnMedica Final piece of type 1 diabetes puzzle solved Overview of type 1 diabetes All pregnant women with type 1 diabetes should be offered continuous glucose monitoring Intensive weight loss can ‘reverse’ type 2 diabetes Five distinct types of diabetes, not just two, suggests study (Source: OnMedica Latest News)
Source: OnMedica Latest News - April 18, 2018 Category: UK Health Source Type: news

MitoCPR--A surveillance pathway that protects mitochondria in response to protein import stress
Mitochondrial functions are essential for cell viability and rely on protein import into the organelle. Various disease and stress conditions can lead to mitochondrial import defects. We found that inhibition of mitochondrial import in budding yeast activated a surveillance mechanism, mitoCPR, that improved mitochondrial import and protected mitochondria during import stress. mitoCPR induced expression of Cis1, which associated with the mitochondrial translocase to reduce the accumulation of mitochondrial precursor proteins at the mitochondrial translocase. Clearance of precursor proteins depended on the Cis1-interacting A...
Source: ScienceNOW - April 12, 2018 Category: Science Authors: Weidberg, H., Amon, A. Tags: Cell Biology, Molecular Biology, Online Only r-articles Source Type: news