Juan C. Landoni

This study shows that NAD+ precursor treatment improves cardiac function but worsens erythroid maturation in mitochondrial progeria, highlighting tissue-specific effects of NAD+ boosting.

The paper identifies MTERF1 as a suppressor of mtDNA deletion pathologies by showing its loss enhances mitochondrial function through transcriptional relief.

The paper investigates asymmetric mitochondrial trafficking in cultured cells, showing it maintains mitochondrial network morphology by balancing perinuclear biogenesis.

The paper shows that mitochondrial DNA nucleoid distribution is controlled by pearling and cristae structure, revealing a mechanism for nucleoid spacing and segregation.

This paper introduces qExM, a method to estimate endogenous protein abundance in expanded samples, achieving a 9.4% mean percent error in nuclear pore complex subunit stoichiometry.

This paper introduces hybrid-EDA, a microscopy framework that reduces phototoxicity while capturing rare biological events using event-driven fluorescence acquisitions.

This study identifies a biophysical mechanism for mitochondrial pearling, showing it occurs spontaneously in various cell types and is driven by internal pressure or external tension.

This study shows that overactive mitochondrial DNA replication causes neonatal heart failure through ferroptosis by disrupting cardiac maturation and oxidative metabolism.