The registrations for Targeting Mitochondria 2017 World Congress are now open!
On behalf of the Scientific Committee of World Mitochondria Society, we are pleased to inform you that the 8th World Congress on Targeting Mitochondria will be organized on October 23 and 24, 2017 at Steigenberger Hotel, in Berlin.
You can now register to the congress with the very early bird rates before March 21, at midnight, by clicking here.
You can also submit your abstract until September 14 for short oral presentation and until September 28 for poster presentation here.
We look forward to meeting you in Berlin next October.
World Mitochondria Society
www.targeting-mitochondria.com
Presentation of the mitochondrial DNA damaged induced inflammation in lung epithelial cells
Dr Bartosz Szczesny, Associate Professor at the Department of Anesthesiology of the University of Texas Medical Branch at Galveston, USA is invited during Targeting Mitochondria World Congress is to give a presentation about the mitochondrial DNA damaged induced inflammation in lung epithelial cells.
According to Dr Szczesny: "Pulmonary epithelial cells are key effectors and targets in the pathogenesis of inflammatory lung diseases such as asthma, and chronic obstructive pulmonary disease, among others. Oxidative stress has been implicated at the earliest step in development of lung inflammation, but the molecular mechanisms of how oxidantive injury to epithelial cells develops inflammatory response remain unclear. While investigating the mechanisms responsible for activating inflammation in response to prolonged, low-level oxidative stress, we identified a role for an active and selective cellular extrusion of damaged mitochondrial DNA, that did not affect cellular viability. Selective release of damaged mitochondrial DNA, first into the cytoplasm and subsequently into the extracellular space, triggers autocrine and paracrine modes of the inflammatory response. I will be discussing cellular outcomes and inflammatory signaling pathways in response to mitochondrial DNA-specific damage in cell culture and in vivo models."
More information about the congress: www.targeting-mitochondria.com
Self-Assembled Polymeric Nanoparticle for Mitochondria-Targeting Drug Delivery
Dr Han Chang Kang, from the Department of Pharmacy, The Catholic University of Korea, Republic of Korea will present his recent research about the Self-Assembled Polymeric Nanoparticle for Mitochondria-Targeting Drug Delivery.
Recently, subcellular targeting drug delivery systems that specifically reach subcellular compartments (e.g., cytosol, nucleus, and mitochondria) of interest have garnered more attention because their action sites for generating therapeutic effects occur not just at the cellular level but at the subcellular level as well. Among them, this presentation will be focused on mitochondria-targeting self-assembled polymer-based nanoparticles for intracellular drug delivery because mitochondria are very significant intracellular organelles for controlling the homeostasis of vital physiological functions and synthesizing bioenergy molecules and their dysfunction leads to a variety of human disorders including neurodegenerative, neuromuscular, cardiac, and metabolic diseases. The significance of the mitochondria in disease allows a broad spectrum of therapeutics to strengthen or weaken their intrinsic or newly-introducing functions. Thus, the presentation will introduce the mitochondria-targeting drug delivery systems designed by me and my collaborators.
For more information about Targeting Mitochondria Congress: www.targeting-mitochondria.com
What is the impact of mitochondria-targeted antioxidants on cancer progression?
ROS can be produced at different sites in cells: it can be formed in the plasma membrane, the cytosol, but the main ROS generator is the electron transport chain (ETC) located in the mitochondrial matrix. Interestingly, enhanced or disrupted mitochondrial activity can increase superoxide production within the mitochondria of cancer cells. The increased superoxide production has been associated with cell survival and metastasis. Thus, it has been hypothesized that specifically targeting mitochondrially-produced ROS could reduce the survival and invasive abilities of cancer cells. Consequently, several mitochondrial antioxidants have been developed and tested; but thus far, no studies have defined the impact of mitochondria-targeted antioxidants on the progression of cancer in endogenous mouse models.
In this talk, Pr Martin Bergö from Sahlgrenska Cancer Center, Sweden, will give an update of their experiments designed to address this issue.
For more information about Targeting Mitochondria Congress: www.targeting-mitochondria.com
iPSC-based drug discovery for neurological mitochondrial disease: presentation of recent scientific data
Mitochondrial DNA (mtDNA) mutations frequently cause neurological diseases. Modeling of these defects has been difficult because of the challenges associated with engineering mtDNA. Patient-derived induced pluripotent stem cells (iPSCs) allow the development of innovative cellular models in a personalized approach.
During Targeting Mitochondria World Congress, Dr Alessandro Prigione from Max Delbrueck Center for Molecular Medicine, Germany will discuss the potential benefits of patient iPSCs for drug discovery of neurological mitochondrial diseases.
To access to the preliminary agenda, please click here.
Dr Yuri Takeda will talk about the prevention of mitochondrial disease transmission
Dr. Yuko Takeda from The Newcastle University, United Kingdom will participate to the Targeting Mitochondria World congress 2017 and present her & her team's study on "Early pronuclear transfer to prevent mitochondrial DNA disease".
According to Dr Takeda, the mutations in mitochondrial DNA (mtDNA) are maternally transmitted and are associated with a broad range of debilitating and fatal multisystem diseases. There are currently no effective treatments for mtDNA disease, however, there has been much interest in the potential of reproductive technologies to prevent transmission. One approach involves the transfer of pronuclei from the fertilized egg of an affected woman to that of a healthy donor, termed pronuclear transfer (PNT).
More information about the congress: www.targeting-mitochondria.com
Mitochondrial ROS and longevity: Recent scientific advances
Ana Lechuga-Vieco, researcher from Fundación Centro Nacional de Investigaciones Cardiovasculares, Spain will talk about her study on "Mitochondrial ROS and longevity: Recent scientific advances" during 8th World congress on Targeting Mitochondria.
According her reseach, she summarize her talk: "Animal models with identical nuclear genomes but with different mtDNA haplotypes (conplastic mice) generate functionally different OXPHOS systems that shape the organismal metabolism, supporting the conclusion that different mtDNA wild type haplotypes are phenotypically relevant. We report that mtDNA haplotype profoundly influences reactive oxygen species generation, energy homeostasis metabolism, and ageing parameters among others, resulting in different healthy longevities of conplastic strains. The existence of intrinsic mismatch between mtDNA and nDNA reveals lifelong metabolic consequences."
For more information, please visit www.targeting-mitochondria.com
Mitochondrial dysfunction play a key role in the pathophysiology of Alzheimer Disease
Dr Natalia Stefanova, from the Institute of Cytology and Genetics, Novosibirsk, Russia will tell about their recent experimental research that support that mitochondrial dysfunction play a key role in the pathophysiology of Alzheimer Disease (AD) and that therapies with target mitochondria are potent to normalize a wide range of cellular signaling processes and therefore slow the progression of AD. She studied the role of mitochondria in the pathophysiology of this disorder using OXYS rats that simulate key characteristics of sporadic AD. It was shown that treatment with mitochondria-targeted SkQ1 via improvement of structural and functional state of mitochondria is able to alleviated the structural neurodegenerative alterations, prevented the neuronal loss and synaptic damage, increased the levels of synaptic proteins, enhanced neurotrophic supply, and decreased amyloid-β1-42 protein levels and tau hyperphosphorylation in the hippocampus of OXYS rats, resulting in improvement of the learning ability and memory.
More information: www.targeting-mitochondria.com
