The congress brings together experts to explore mitochondria's role in cellular dynamics, metabolic control, and therapeutic targets. Key findings include the emergence of mitochondria as biological sensors and decision-makers, translating environmental signals into cellular fate.
The 17th World Congress on Targeting Mitochondria will gather world's leading experts from biotechnology, pharma and academia to discuss health, longevity and precision medicine. Over 150 academic and institutional partners and 30 industrial and investment organizations are participating.
Researchers will explore the intersection of mitochondria and microbiota through extracellular vesicles for diagnostics, targeted drug delivery, and regenerative medicine. The conference aims to accelerate scientific progress by building bridges between disciplines.
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Researchers discovered that mitochondrial dysfunction triggers a sophisticated metabolic response in brown fat cells, rewiring key enzymes to produce D-2HG. This metabolite modifies the cell nucleus, changing gene expression and nuclear structure, promoting adaptation and altering cellular identity.
Researchers discovered that Osteopontin induces mitochondrial biogenesis in deadherent breast tumor cells, which aids metastatic success. The study suggests a possible mechanism and targets for treating cancer metastasis by increasing ATP levels and mitochondrial mass.
Researchers discovered that a conserved receptor molecule called Tom70 coordinates the balance between protein production and import into mitochondria. This finding ties to increased lifespan and delayed mitochondrial dysfunction when Tom70 levels are elevated. The study provides new insights into aging and age-related diseases.
Researchers found early mitochondrial biogenesis deficits in individuals with Friedreich's ataxia, suggesting a potential biomarker and therapeutic target. Early intervention may prove crucial to successful therapy for this rare genetic disorder.
Researchers found that carbon monoxide inhalation restores mitochondrial biogenesis in doxorubicin-treated mice, preventing cardiomyopathy. Overexpression of the protein HO-1 also reduced mitochondrial DNA damage and cell death in rat cardiac cells.
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