Beyond mitochondria: Alternative energy-producing pathways from all strata of life

Mitochondrial substrate level phosphorylation via succinate-CoA ligase enables survival despite a defective electron transport chain.

This brilliant study by Christopher Auger et. al reviews alternative energy-producing pathways from all strata of life.

Mitochondria are the powerhouses of the cell for they produce adenosine triphosphate (ATP), the universal energy currency. However, intricacy and efficiency, the most significant strengths of the electron transport chain (ETC), are also its greatest downfalls.

A reliance on metal complexes, lipid moities, and cofactors renders oxidative phosphorylation vulnerable to environmental toxins, intracellular reactive oxygen species (ROS) and fluctuations in diet. Thus, it is of interest to note that temporal disruptions in ETC activity in most organisms are rarely fatal, and often a redundant number of failsafes are in place to permit continued ATP production when needed.

This review highlights the metabolic reconfigurations discovered in organisms ranging from parasitic Entamoeba to bacteria such as pseudomonads and then complex eukaryotic systems that allow these species to adapt to and occasionally thrive in harsh environments.

The aim of this review is to demonstrate the plasticity of metabolic networks and recognize that in times of duress, life finds a way.

The author of this paper, Dr. Marc G. Jeschke, will join us during the 13th World Congress in October to present all his recent results concerning mitochondrial function and associate metabolic changes in a model of severe trauma

Read more about this article: 10.1016/j.metabol.2021.154733

Targeting Mitochondria 2022 Congress
October 26-28, 2022 - Berlin, Germany 
www.targeting-mitochondria.com

How regular exercise can protect against fatty liver associated diseases

Exercise prevents fatty liver by modifying the compensatory response of mitochondrial metabolism to excess substrate availability. Credit: DZD

An illuminating study conducted by the German Center for Diabetes Research (DZD), Helmholtz Munich and Tübingen University Hospital elucidates how exercise can protect against fatty liver disease.

Worldwide one in four persons suffers from non-alcoholic liver disease (NAFLD, also called metabolic liver disease MAFLD). Those affected often have type 2 diabetes as well as an increased risk of liver cirrhosis and cardiovascular diseases. In addition, NAFLD is associated with increased mortality. An imbalance between energy intake and consumption is discussed as a cause for the disease. This leads to fat deposits in the liver and over time impairs the function of the mitochondria

To prevent and treat NAFLD, lifestyle modification with increased physical activity is recommended. To what extent regular exercise alters the adaptation of the liver to increased energy intake and what role skeletal muscle plays in this process was investigated by scientists at the Institute of Clinical Chemistry and Pathobiochemistry at Tübingen University Hospital and at the Institute of Diabetes Research and Metabolic Diseases (IDM) of Helmholtz Munich at the University of Tübingen.

The results showed that training regulated important enzymes of glucose and fructose degradation in the liver as well as the mitochondrial pyruvate metabolism. In this way, the substrate burden for mitochondrial respiration and lipid synthesis can be reduced. As a consequence, less fat is stored in the liver – and specific lipids such as diacylglycerol species are lowered. Moreover, glucose control improves in the exercise trained mice. In addition, an increased respiratory capacity of the skeletal muscles relieves the metabolic stress in the liver. 

Stay tuned and explore the latest researches in science.

Read more

Original Article

Mitochondrial Transfer in Cardiovascular Disease: From Mechanisms to Therapeutic Implications

Therapeutic strategies of mitochondrial transfer for cardiovascular diseases.

This informative review by Chen et al. studied the phenomenon of mitochondrial transfer in cardiovascular diseases.

Mitochondrial dysfunction has been proven to play a critical role in the pathogenesis of cardiovascular diseases. The phenomenon of intercellular mitochondrial transfer has been discovered in the cardiovascular system. This cell-to-cell mitochondrial transfer plays an essential role in regulating cardiovascular system development and maintaining normal tissue homeostasis under physiological conditions. In pathological conditions, damaged cells transfer dysfunctional mitochondria toward recipient cells to ask for help and take up exogenous functional mitochondria to alleviate injury.

In this review, they summarized the mechanism of mitochondrial transfer in the cardiovascular system and outlined the fate and functional role of donor mitochondria. They also discussed the advantage and challenges of mitochondrial transfer strategies, including cell-based mitochondrial transplantation, extracellular vesicle-based mitochondrial transplantation, and naked mitochondrial transplantation, for the treatment of cardiovascular disorders.

This topic and many more are to be presented in our 13th Annual Meeting 2022 - in Germany

Authors: Jun Chen, Jinjie Zhong, Lin-lin Wang, and Ying-ying Chen

Read full article.

Two Blood Markers of Schizophrenia Identified

Mouse parvalbumin neurons. Credit: @UNIL/CHUV Inès Khadimallah

This phenomenal research by Synapsy brings us closer to diagnosing Schizophrenia by blood, and treating it. 

A research team from Synapsy has shown that the severity of the clinical symptoms of schizophrenia is strongly linked to blood biomarkers related to the deregulation of neuronal mitochondria.

A study conducted at the Centre for Psychiatric Neuroscience of the Lausanne University (UNIL) and the Lausanne University Hospital (CHUV), and supported by the National Centre of Competences in Research Synapsy (Synapsy), has shown, in an animal model, that the cellular mechanism for recycling mitochondria is deficient in parvalbumin neurons.

Mitochondria are generally able to eliminate their damaged parts by splitting, using a mechanism called mitophagy. This process involves a series of molecules whose production is controlled by miR137, a microRNA that plays a key role in their regulation. Inès Khadimallah, in collaboration with her colleagues, succeeded in demonstrating that the level of miR-137 was very high in the model, as was oxidative stress. In parallel, an element of cellular respiration expressed specifically by parvalbumin neurons, the COX6A2 molecule is decreased. "In other words, the mitochondria of parvalbumin neurons are dysfunctional following the increase in oxidative stress, and it can be shown through analyzing the levels of miR-137 and COX6A2 in the blood".

In their attempts to intervene directly on the free radicals produced by mitochondria, the neuroscientists showed, in the animal model, that the alterations of these two molecules, miR137 and COX6A2, can be completely corrected by an antioxidant compound that specifically targets mitochondria, called MitoQ.

Keep on track with us and stay updated with all the latest research!

Read more.

Access full article