Mitochondria and Cell Death Regulation following toxic injury

Programme Leader: L. Miguel Martins

Summary of Research Interests

Our work focuses on mitochondrial signaling pathways of toxicity associated with neurodegenerative diseases. Understanding the basic biology of these processes can give insights that are aimed to deliver field-changing mechanistic insights into toxicology and disease.

The aim of this work is to target these pathways to improve neuronal health in models of Parkinson’s disease and other diseases related to mitochondrial dysfunction. We use the fruit fly as a model to study organs and tissues with high energetic demand, such as the brain and muscles susceptible to toxic insults.

Video summaries of our latest research:



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Recent research publications:

Lehmann, S. et al. Folinic acid is neuroprotective in a fly model of Parkinson’s disease associated with pink1 mutations, matters (in press)

Celardo, I. et al. dATF4 regulation of mitochondrial folate-mediated one-carbon metabolism is neuroprotective, Cell Death and Differentiation (2017)

Lehmann, S. et al. Enhancing NAD+ salvage metabolism is neuroprotective in a PINK1 model of Parkinson’s disease. Biology Open (2016)

Sood, P. et al. Paraquat-induced metabolic stress signature in human foetal mesencephalic cells. matters (2016)

Celardo, I. et al. Mitofusin-mediated ER stress triggers neurodegeneration in pink1/parkin models of Parkinson’s disease, Cell Death and Disease (2016)

Lehmann, S. et al. Parp mutations protect against mitochondrial dysfunction and neurodegeneration in a PARKIN model of Parkinson’s disease. Cell Death and Disease (2016)

Bartesaghi, S. et al. Inhibition of oxidative metabolism leads to p53 genetic inactivation and transformation in neural stem cells. PNAS (2015)

Andree, M. et al. BID-dependent release of mitochondrial SMAC dampens XIAP-mediated immunity against Shigella. The EMBO Journal (2014)

Requejo-Aguilar, R. et al. PINK1 deficiency sustains cell proliferation by reprogramming glucose metabolism through HIF1. Nature Communications 5, 1–9 (2014)

Tufi, R. et al. Enhancing nucleotide metabolism protects against mitochondrial dysfunction and neurodegeneration in a PINK1 model of Parkinson’s disease. Nature Cell Biology  (2014)

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