Education:

Pharmacy Degree (“Pharmazeutische Prüfung”), Düsseldorf University, 1981
Ph.D. in pharmacology, Düsseldorf University, 1985
Post-doctoral fellowship in cell signaling, Stanford University, 1987

Positions and Employment:

Honors and Awards:

Research Interests:

Dr. Schroeder’s research focuses on the regulation of antioxidant proteins and their potential role as therapeutic targets in atherosclerosis.  One of these candidate proteins is heme oxygenase-1 (HO-1) which degrades heme and generates bilirubin and carbon monoxide (CO).  Both products have strong antioxidant and anti-inflammatory properties.  CO, in addition, acts as a dilator of blood vessels.  HO-1 has been shown to be a target and mediator of established drugs such as aspirin, the statins, and organic nitrates (nitric oxide donors).  Recent data indicate that some bioactive peptides (e.g., derived from fish or soy) and other micronutrients function as inducers of HO-1 which may explain their antioxidant and antihypertensive properties.

Although a number of agents induce HO-1 via nitric oxide and cyclic nucleotides (cGMP / cAMP), Dr. Schroeder’s lab has demonstrated the existence of additional, as yet unexplored, pathways.  His research team continues to characterize the various signaling routes and mediators involved in HO-1 expression and to study their relevance in the treatment of cardiovascular disease and other inflammatory processes such as ischemia and reperfusion injury, Alzheimers disease, transplant rejection, and autoimmume disorders (e.g., rheumatoid arthritis, psoriasis).

Functionally, increased expression of HO-1 leads to protection from oxidant injury in endothelial cells and to a reduction in renal toxicity of immunosuppressants such as cyclosporin A.  Besides examining transcriptional and translational regulation, Dr. Schroeder’s group is also monitoring the changes in the formation of downstream products and mediators such as bilirubin and ferritin.  The ultimate goals of these studies are to explore the underlying molecular mechanisms and, more importantly, to find clinical markers for the induction of antioxidant genes.

Selected publications:

Muchova L., Wong R.J., Hsu M., Morioka I., Vitek L., Zelenka J., Schröder H. and Stevenson DK (2007) Chronic statin treatment increases formation of carbon monoxide and bilirubin in mice: a novel mechanism of antioxidant protection.  Can. J. Physiol. Pharmacol. (in press).

Rothkegel C., Atkins D.-J., Schmidt P.M., Schröder H., Schmidt H.H.H.W. and Stasch J.-P. (2007) Characterization of the a₁/ß₁ dimerization region of soluble guanylyl cyclase by bimolecular fluorescence complementation.  Mol. Pharmacol. (in press).

Erdmann K., Grosser N., Schipporeit K. and Schröder H. (2006) The ACE inhibitory dipeptide Met-Tyr diminishes free radical formation in human endothelial cells via induction of heme oxygenase-1 and ferritin.  J. Nutr. 136: 1-5.

Schröder H. (2005) Novel pathways for an old drug: lipoxin A4 may mediate heme oxygenase-1 induction by aspirin.  Am. J. Physiol. Cell. Physiol. 289: C507-C508.

Schmidt P., Schramm M., Schröder H., Wunder F., Stasch J.-P. (2004) Identification of residues crucially involved in the binding of the heme moiety of soluble guanylate cyclase.  J. Biol. Chem. 279: 3025-3032.

Grosser N., Hemmerle A., Berndt G., Erdmann K., Hinkelmann U., Schürger S., Wijayanti N., Immenschuh S. and Schröder H. (2004) The antioxidant defense protein heme oxygenase-1 is a novel target for statins in endothelial cells.  Free Radic. Biol. Med. 37: 2064-2071.

Grosser N. and Schröder H. (2003) Aspirin protects endothelial cells from oxidant damage via the nitric oxide-cGMP pathway.  Arterioscler. Thromb. Vasc. Biol. 23: 1345-1351.

Polte T., Hemmerle A., Berndt G., Grosser N., Abate A., and Schröder H. (2002) Atrial natriuretic peptide reduces cyclosporin toxicity in renal cells: role of cGMP and heme oxygenase-1.  Free Radic. Biol. Med. 32: 56-63.