Stefan W. Ryter

Heme oxygenase/carbon monoxide signaling pathways: regulation and functional significance.

Mitogen activated protein kinase (MAPK) pathway regulates heme oxygenase-1 gene expression by hypoxia in vascular cells.

Heme oxygenase-1: molecular mechanisms of gene expression in oxygen-related stress.

Necrotic cell death in response to oxidant stress involves the activation of the apoptogenic caspase-8/bid pathway.

Heme oxygenase-1 and carbon monoxide in pulmonary medicine.

Analysis of pulmonary heme oxygenase-1 and nitric oxide synthase alterations in experimental hepatopulmonary syndrome.

Hepatocyte growth factor protects against hypoxia/reoxygenation-induced apoptosis in endothelial cells.

Carbon monoxide in biology and medicine.

Carbon monoxide: to boldly go where NO has gone before.

Caveolae compartmentalization of heme oxygenase-1 in endothelial cells.

Bcl-XL disrupts death-inducing signal complex formation in plasma membrane induced by hypoxia/reoxygenation.

Heme oxygenase-1: redox regulation of a stress protein in lung and cell culture models.

FLIP protects against hypoxia/reoxygenation-induced endothelial cell apoptosis by inhibiting Bax activation.

Caveolin-1 expression by means of p38beta mitogen-activated protein kinase mediates the antiproliferative effect of carbon monoxide.

Heat shock protein-70 mediates the cytoprotective effect of carbon monoxide: involvement of p38 beta MAPK and heat shock factor-1.

CO as a cellular signaling molecule.

Therapeutic applications of carbon monoxide in lung disease.

Heme oxygenase-1/carbon monoxide: from basic science to therapeutic applications.

Carbon monoxide and bilirubin: potential therapies for pulmonary/vascular injury and disease.

Carbon monoxide differentially inhibits TLR signaling pathways by regulating ROS-induced trafficking of TLRs to lipid rafts.

Mitochondrial localization and function of heme oxygenase-1 in cigarette smoke-induced cell death.

Mechanisms of cell death in oxidative stress.

Carbon monoxide protects against hyperoxia-induced endothelial cell apoptosis by inhibiting reactive oxygen species formation.

Hemodynamic and molecular response to intermittent hypoxia (IH) versus continuous hypoxia (CH) in normal humans.

Cytoprotective and anti-inflammatory actions of carbon monoxide in organ injury and sepsis models.

FLIP inhibits endothelial cell apoptosis during hyperoxia by suppressing Bax.

Thioredoxin catalyzes the denitrosation of low-molecular mass and protein S-nitrosothiols.

Carbon monoxide in sepsis.

Protective functions of heme oxygenase-1 and carbon monoxide in the respiratory system.

Nitric oxide-deficiency regulates hepatic heme oxygenase-1.

Functional significance of apoptosis in chronic obstructive pulmonary disease.

Mitogen-activated protein kinases regulate susceptibility to ventilator-induced lung injury.

Caveolin-1: a critical regulator of pulmonary vascular architecture and nitric oxide bioavailability in pulmonary hypertension.

Deletion of caveolin-1 protects against oxidative lung injury via up-regulation of heme oxygenase-1.

Protein kinase C alpha and zeta differentially regulate death-inducing signaling complex formation in cigarette smoke extract-induced apoptosis.

Carbon monoxide protects against ventilator-induced lung injury via PPAR-gamma and inhibition of Egr-1.

Inducing hypoxemia in healthy humans: a method for intermittently lowering arterial blood oxygenation during physiological studies.

Autophagic proteins regulate cigarette smoke-induced apoptosis: protective role of heme oxygenase-1.

Network analysis of temporal effects of intermittent and sustained hypoxia on rat lungs.

Egr-1 regulates autophagy in cigarette smoke-induced chronic obstructive pulmonary disease.

Identifying targets for COPD treatment through gene expression analyses.

Autophagy in chronic obstructive pulmonary disease: homeostatic or pathogenic mechanism?

Analyzing autophagy in clinical tissues of lung and vascular diseases.

The heme oxygenase-1/carbon monoxide pathway suppresses TLR4 signaling by regulating the interaction of TLR4 with caveolin-1.

Carbon monoxide prevents ventilator-induced lung injury via caveolin-1.

Heme oxygenase-1, a critical arbitrator of cell death pathways in lung injury and disease.

Heme oxygenase-1/carbon monoxide: from metabolism to molecular therapy.

Autophagy in the lung.

Autophagy in vascular disease.

Inhaled hydrogen sulfide protects against ventilator-induced lung injury.

Heme oxygenase-1/carbon monoxide: novel therapeutic strategies in critical care medicine.

Evaluation of inhaled carbon monoxide as an anti-inflammatory therapy in a nonhuman primate model of lung inflammation.

Autophagic protein LC3B confers resistance against hypoxia-induced pulmonary hypertension.

Autophagy in cigarette smoke-induced chronic obstructive pulmonary disease.

Autophagy protein microtubule-associated protein 1 light chain-3B (LC3B) activates extrinsic apoptosis during cigarette smoke-induced emphysema.

Autophagy proteins regulate innate immune responses by inhibiting the release of mitochondrial DNA mediated by the NALP3 inflammasome.

Deadly triplex: smoke, autophagy and apoptosis.

Exhaled carbon monoxide as a biomarker of inflammatory lung disease.

Special issue on carbon monoxide and exhaled biomarkers in human disease.

Carbon monoxide activates autophagy via mitochondrial reactive oxygen species formation.

Carbon monoxide, a reaction product of heme oxygenase-1, suppresses the expression of C-reactive protein by endoplasmic reticulum stress through modulation of the unfolded protein response.

Beclin 1 deficiency is associated with increased hypoxia-induced angiogenesis.

Autophagy in pulmonary diseases.

Hyperoxia Induced LC3B Interacts with the Fas Apoptotic Pathway in Epithelial Cell Death.

Carbon monoxide inhibits Fas activating antibody-induced apoptosis in endothelial cells.

Autophagy in inflammatory diseases.

Heme Oxygenase-1/CO as Protective Mediators in Cigarette Smoke-Induced Lung Cell Injury and Chronic Obstructive Pulmonary Disease.

Statins and Pulmonary Fibrosis: The Potential Role of NLRP3 Inflammasome Activation.

Pretreatment with carbon monoxide releasing molecules suppresses hepcidin expression during inflammation and endoplasmic reticulum stress through inhibition of the STAT3 and CREBH pathways.

Autophagic proteins: New facets of the oxygen paradox.