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Research activities

Our research group focuses on the intricate connection between mitochondrial function, metabolic routes, signal transduction pathways and gene expression.


We have described interdependence between PARP-1, PARP-2 and SIRT1. The depletion of PARP-1, or PARP-2 enhance SIRT1 activity. The depletion of PARP-2 acts via activating SIRT1 promoter, while depletion of PARP-1 activates SIRT1 via enhancing cellular NAD+ levels. The consequent induction of SIRT1 induces mitochondrial biogenesis in various tissues leading to the improvement of insulin sensitivity. PARP inhibitor treatment brought about a similar, metabolicly advantageous phenotype.


The depletion of PARP-2 provided protection against Doxorubicin-induced vascular dysfunction. We have shown that the depletion of PARP-2 stabilizes Doxorubicin-damaged mitochondria through SIRT1 activation. Preservation of mitochondrial function protect damaged vascular smooth muscle cells.