Progressive neurodegenerative diseases affect millions of people worldwide. As mitochondrial/ER dysfunction and inflammation are responsible for the initiation and progression of the neuropathology, proteins that prevent deregulation of both pathways are considered as drug targets.

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Our laboratory aims at identifying the molecular mechanisms responsible for cell death (particularly ferroptosis) and at elucidating their involvement in human diseases. To achieve this goal, we combine experimental strategies with focused pharmacological, genetic, biochemical, and physiological studies of mitochondrial functions and inflammation in rodent and human cells.

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Potential therapeutic approaches may benefit from modulation of small-conductance calcium-activated potassium (SK) channels, since recent data supports the hypothesis that SK channel activity promotes neuronal survival against cellular stress via a dual mechanism of action: i) by controlling neuronal excitability, and ii) by preventing mitochondrial dysfunction and inflammation.