Pablo Hernansanz‐Agustín

The paper shows that modifying ionic interactions with phospholipids prevents hypoxic adaptation by preserving inner mitochondrial membrane fluidity and CoQ transfer.

This study shows that loss of HIF1α in smooth muscle cells in atherosclerosis leads to oxidative stress, increased SMC proliferation, and plaque expansion.

This study shows TET3 regulates terminal differentiation by affecting mitochondrial metabolic maturation and oxidative phosphorylation in intestinal epithelial cells.

The paper shows that tafazzin deficiency in Barth Syndrome protects against ferroptosis by altering mitochondrial cardiolipin metabolism, affecting VDAC function and reducing ROS availability for ferroptosis.

This study shows that NCLX is necessary for HIF-1 stabilization and transcriptional activity during hypoxia, linking acute and medium-term hypoxic responses through mitochondrial signaling.

This study investigates the role of SCAF1 in mitochondrial respiratory supercomplexes in mice, showing its structural role in respirasome formation and its impact on respiration and ROS production.

The paper identifies SIN3A's role in hypoxia-induced transcriptional changes, showing it represses 75% of hypoxia-repressed genes and inhibits 47% of hypoxia-induced genes.