Cristiane Benincá

The paper screens FDA-approved compounds to find mitophagy activators, identifying Meptazinol and Ponatinib as top candidates that increase mitolysosomes but do not rescue bioenergetic defects in mitochondrial diseases.

This study identifies Gαq as a regulator of mitochondria-lysosome contact dynamics, showing its role in mitochondrial fragmentation and quality control through interactions with Fis1 and RabGAPs.

This paper identifies that truncating variants in KAT6A cause two distinct neurodevelopmental disorders with opposing gene regulatory and metabolic effects, highlighting the need for variant-level stratification in therapy development.

This paper shows that activating the MasR receptor with CAP-1902 improves mitochondrial function in a human Complex III deficiency model by enhancing turnover and reducing stress.

This study shows that reduced oxidative phosphorylation is not required for pro-inflammatory macrophage activation, challenging the conventional model of mitochondrial reprogramming.

The paper shows BT2 acts as a mitochondrial uncoupler, reducing ROS and lipogenesis, which may explain its therapeutic benefits in metabolic diseases.

This study shows neural stem cells transfer functional mitochondria via extracellular vesicles to restore mitochondrial function in target cells, improving disease outcomes in multiple sclerosis.