David A. Hanna

This study shows hydrogen sulfide increases copper uptake and localization in cells, with copper primarily in the Cu2+ state, using the ZNT1 transporter for import and ATP7A for export.

This study identifies a heme-SDH-CoQ axis that helps colorectal cancer cells resist iron-induced oxidative stress and cell death.

The paper identifies fedratinib as a drug that increases endoplasmic reticulum-mitochondria contact sites by inhibiting BRD4, revealing a novel epigenetic pathway linking ERMCS to cellular metabolism.

This study shows hydrogen sulfide increases intracellular oxygen and destabilizes HIF-1, altering hypoxia sensing and potentially contributing to O2 toxicity diseases.

This study shows that chronic hydrogen sulfide exposure alters mitochondrial structure and function in human cells by disrupting cristae and respiratory supercomplexes.

This study shows that H2S preconditioning causes long-lasting changes in O2 metabolism, including increased P50(O2) and metabolic memory effects lasting up to 24-48 hours.