Jawed Alam

TL;DR: The molecular and biochemical characterization of HOs is reviewed, with a discussion on the mechanisms of signal transduction and gene regulation that mediate the induction of HO-1 by environmental stress, to lay a foundation for potential future clinical applications of these systems.

TL;DR: It is demonstrated here that carbon monoxide, a by-product of heme catabolism by heme oxygenase, mediates potent anti-inflammatory effects and may have an important protective function in inflammatory disease states and thus has potential therapeutic uses.

TL;DR: Results implicate Nrf2 in the induction of the HO-1 gene but suggest that the NRF2 partner in this function is a factor other than p18 or Jun proteins.

TL;DR: The magnitude ofHO-1 induction after oxidative stress and the wide distribution of this enzyme in systemic tissues coupled with the intriguing biological activities of the catalytic byproducts, carbon monoxide, iron, and bilirubin makes HO-1 a highly attractive and interesting candidate stress-response protein which may play key role(s) in mediating protection against oxidant-mediated lung injury.

TL;DR: Data demonstrate that hypoxia induces HO-1 expression in animal tissues and cell cultures and implicate HIF-1 in this response.