The Future of Medicine will come through Mitochondria


Prof. Volkmar WeissigWe are excited to invite you to the 17th World Mitochondria Scoiety's Annual Meeting, happening from October 21–23, 2026, in Berlin. This annual event brings together top experts in mitochondrial research and medicine to share new discoveries and ideas in mitochondrial therapy, gene treatment, and mitochondrial transplantation.

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WMS is pleased to award Dr. Igor Sobenin for his Poster Presentation

Poster-award

On behalf of the Scientific Committee, we congratulate Dr. Igor Sobenin from Russian Cardiology Research and Production Complex, Russian Federation for his award for Poster Presentation during Targeting Mitochondria World Congress which was held in Berlin, Germany.

Dr. Igor Sobenin has presented a Poster about "Association of Mitochondrial Mutations with Sublinical Carotid Atherosclerosis".

According Dr. Igor Sobenin: "In human pathology, several diseases are associated with somatic mutations in the mitochondrial genome (mtDNA). Even though mitochondrial dysfunction leads to increased oxidative stress, the role of mitochondrial mutations in atherosclerosis has not received much attention so far. Mitochondrial mutations may be one of the causes of atherosclerosis development in human arteries. Recently we have found that at least 10 mitochondrial mutations in 8 genes (rRNA 12S, 2 genes tRNA-Leu (codons recognized UUR and CUN), cytochrome B, and subunits 1, 2, 5, and 6 NADH dehydrogenase) had higher frequency in atherosclerotic plaques as compared to normal intima. The aim of present research was to reveal the association of the above mutations occurring in mitochondrial genome with the extent of subclinical carotid atherosclerosis. We have analyzed the association of mitochondrial genetic variation with the severity of carotid atherosclerosis, as assessed by carotid intima-media thickness (cIMT) and the presence of coronary heart disease (CHD) in 190 subjects from Moscow, Russia, a population with high CHD occurrence. cIMT was measured by high-resolution B-mode ultrasonography, and the level of mtDNA heteroplasmy in human leucocytes was determined by pyrosequencing method adopted for conditions where both mutant and normal allele were present in the same specimen. According to the results of ultrasonographic evaluation, the study participants were classified as non-atherosclerotic (NA), patients with diffuse intima-media thickening (DIT), and patients with subclinical atherosclerosis, who had at least one atherosclerotic plaque in common carotid artery (AP). The level of heteroplasmy was significantly higher for C3256T, G12315A and G15059A mutations in DIT and further in AP as compared to NA. On the opposite, the level of heteroplasmy declined from NA to AP for G13513A and Ins652G mutations. There was a strict linear-linear relationship between the extent of subclinical carotid atherosclerosis and quartiles of heteroplasmy for all above mutations (p<0.001). We found that heteroplasmies for several mutations in the mtDNA in leukocytes, including C3256T, T3336C, G12315A, G13513A, G14459A, G14846A, and G15059A mutations, were significantly (p<0.001) associated with both the severity of carotid atherosclerosis and the presence of CHD. These findings indicate that somatic mitochondrial mutations may play a significant role in the development of atherosclerosis, and demonstrate the evidence for genetic predisposition to atherosclerosis on the level of mitochondrial genome."

For more information about Targeting Mitochondria 2014: www.targeting-mitochondria.com

 

WMS discerned the award of Short Oral Presentation to Dr. Nina Entelis

ShortOral-award

Dr. Nina Entelis,  from University of Stasbourg, France was awarded for her Short Oral Presentation by WMS Scientific Committee during the 5th International Congress on Targeting Mitochondria which was held in Berlin on October 29-30-31.

During Targeting Mitochondria 2014, Dr. Nina Entelis gave a presentation about "Design of therapeutic anti-replicative RNA imported into mitochondria of human cells.".

According Dr. Nina Entelis: "Mutations in mitochondrial genome (mtDNA) have been associated with a wide variety of human disorders. In patients with mtDNA defects, it is common to find mutant and wild type mtDNA molecules in the same cell, the phenomenon known as heteroplasmy. Manifestation of biochemical and clinical defects occurs only when a threshold level of heteroplasmy (generally, >60% of mutant genomes) has been reached. Since there is no efficient treatment for these disorders, one attractive approach would be to specifically target mutant mtDNA and prevent it from replicating, thereby giving an advantage to the propagation of wild type genomes.

This strategy is confronted to two problems: translocation of anti-genomic oligomers through the double mitochondrial membrane, and their access and specific binding to mutated region of mtDNA. Our study of the natural pathway of RNA import into mitochondria permitted to identify the import determinants in tRNA and 5S rRNA structures. Basing on these data, a set of small RNA molecules with significantly improved efficiency of mitochondrial targeting was designed[1,2].

To target therapeutic oligonucleotides into deficient human mitochondria, we inserted short sequences corresponding to the boundaries of a large deletion in mtDNA[3] or to the region of a point mutation[4] into importable RNAs. We demonstrated that recombinant RNA molecules containing determinants for mitochondrial import and 20-nucleotide sequence corresponding to the mutated region of mtDNA, are able to anneal selectively to the mutated mitochondrial genomes. After import into mitochondria of cultured human cells, these RNAs induced a decrease of the proportion of mtDNA bearing a pathogenic mutation.

To improve the stability of anti-replicative RNA molecules in human cells, we introduced into these molecules various chemically modified oligonucleotides and tested their impact on the efficiency of their hybridisation with mtDNA in vitro, RNA stability, mitochondrial targeting and the effect on heteroplasmy in human cybrid cells in culture[5]. We also demonstrated that anti-replicative RNA molecules conjugated with cholesterol are able to penetrate into cultured cells without additional lypophilic agents.

Another way to obtain a shift of heteroplasmy level consists in stable expression of anti-replicative molecules in cells. We therefore developed cybrid cell lines expressing recombinant 5S rRNA molecules and demonstrated an important and stable decrease of their heteroplasmy level.

These studies clearly show that RNA import into mitochondria is a perspective tool suitable for biomedical applications.

This work was supported by the CNRS, Strasbourg University and grants Labex MitoCross, LIA ARN-Mitocure, AFM, ANR, FRM and Suprachem."

 

 

For more information about Targeting Mitochondria 2014: www.targeting-mitochondria.com

 

Pr Martin Kerschensteiner was awarded by the Scientific Committee of World Mitochondria Society for his Scientific Contribution

Martin KerschensteinerIt is an honor to announce the award discerned by The Scientific Committee of WMS to Pr. Martin Kerschensteiner from Medical Center of the University of Munich, Germany for his scientific contribution about "Microscopy enables dynamic and functional analysis of mitochondria in vivo", during Targeting Mitochondria 2014.

According Pr. Martin Kerschensteiner: "Here, I want to discuss how recent advances in light microscopy can improve our understanding of mitochondrial pathology in diseases of the nervous system. Over the recent years we have developed optical approaches that allow us to visualize the structure, dynamic behavior and molecular make-up of mitochondria changes in the living nervous system. I will use our work on traumatic and inflammatory axon damage in the spinal cord as examples to illustrate how these imaging approaches can help us to better understand when and where mitochondrial pathology evolves in neurons, which mechanisms induce it and how it may be prevented."

For more information about Targeting Mitochondria 2014: www.targeting-mitochondria.com

 

The 5th edition of Targeting Mitochondria 2014 was a huge success

Targeting-Mitochondria2014-group

The 5th World Congress on Targeting Mitochondria was held on October 29 to 31, 2014, at Hotel Ritz Carlton, Berlin. It was a huge success gathering more than 460 attendees from 36 countries were welcomed. The participants were coming from various fields: academics, industrials, clinicians...



To access to the pictures
 gallery organized in three parts (workshop and second / third day of conference), please click here.

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The Abstracts book of Targeting Mitochondria 2014 is now available in PDF version

Compte Rendu mitoch

All abstracts accepted by the Scientific Committee of Targeting Mitochondria 2014 are published in the abstracts book of the congress.

The abstracts book contains abstracts of major speakers, short oral presentations and posters presentations (186 pages).

You can order this Abstracts Book in PDF Format by clicking here.

 

 

Pictures and moments of Targeting Mitochondria World Congress 2014

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We are very pleased to share with you a few pictures of the 5th Congress of Targeting Mitochondria 2014, which was held on October 29 to 31, 2014, at Hotel Ritz Carlton, Berlin.

We hope these picture will remind you of the best times of the Congress.

To access to the pictures gallery, please click here.

 

The central role of mitochondrial dysfunction in brain and other tissues pathophysiology evaluated in vivo presented by Prof. Avraham Mayevsky

During the Workshop organized on October 28, 2015, Prof. Avraham Mayevsky from Faculty of Life-Sciences and the Multidisciplinary Brain Research Center, Israel will present The central role of mitochondrial dysfunction in brain and other tissues pathophysiology evaluated in vivo.

 

abraham mayevsky

 

He will talk about : 

  • Historical Overview – The 60 years legacy of Prof. Britton Chance.
  • Brain and Tissue Energy Metabolism and Mitochondrial Function.
  • Why and how to Monitor Mitochondrial NADH redox state in vivo.
  • Multiparametric monitoring of NADH together with other tissue physiological activities.
  • Responses of brain and other tissues to various perturbations in Animal Models.
  • Monitoring of Mitochondrial NADH and microcirculatory blood flow and oxygenation in patients

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Treating cancer like an infectious disease: A strategy presented by Dr Rebecca Lamb during WMS Congress

Rebecca Lamb Cadre2

During the 6th World Congress on Targeting Mitochondria scheduled from October 28 to 30 in Berlin,  Dr Rebecca Lamb from the University of Manchester, UK will give a strategic presentation about Antibiotics that target mitochondria effectively eradicate cancer stem cells, across multiple tumor types: Treating cancer like an infectious disease.

Dr Lamb and her team proposes a new strategy for the treatment of cancer, via the selective targeting of cancer stem cells (CSCs) responsible for tumour-initiation, progression, treatment resistance and disease recurrence. They utilized CSC activity as a global phenotypic characteristic of multiple tumour types, to provide a mutation-independent approach to cancer therapy, effectively treating cancer as a single disease of “stemness”.

If you would like to know more about the presentation from Dr Lamb, don't hesitate to register for Targeting Mitochondria World Congress.

More information on www.targeting-mitochondria.com

 

Mitochondria in the Press & Media