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Mitochondria are highly dynamic organelles that play a central role in the cellular metabolism. The classical function to generate energy (ATP) supported by mitochondrial respiration relies on the availability of NADH and FADH2 from tricarboxylic acid (TCA) cycle. Recent evidence demonstrate that TCA cycle activity is highly dependent on calcium uptake provided from endoplasmic reticulum-mitochondria communication mediated by InsP3 receptor and MCU complex. Mitochondria can oxidize glucose-derived pyruvate, lactate, fatty acids,and glutamine according to the cellular requirements and the ability of rewiring these pathways contributes to the pathophysiology of non-communicable diseases such as thrombosis risk and cancer. A diversity of metabolic phenotypes is recognized by controlling the ROS production, epigenetics, biosynthesis, and cell fate; however, the precise regulatory mechanisms remains poorly understand.

Although active research on mitochondrial metabolism of cancer cells has highlighted their unexpected roles during cancer proliferation, metastasis, and chemoresistance; the molecular signaling remain less well known. Therefore, the study of adaptive responses based on metabolic plasticity offers the opportunity to identify new therapeutic targets, expanding the molecular insights for cancer drug discovery.

The aims of MPB lab are:

  • To investigate signaling pathways involved in the control of metabolic plasticity and rewiring of the mitochondrial bioenergetics during proliferation, migration/invasion and chemoresistance of cancer cells.
  • To identify new compounds that interfering the mitochondrial bioenergetics as potential anti-platelet and anti-cancer approaches.
  • To investigate the role of cellular metabolism on the effects of FDA-approved drugs.