Ethan Anderson, PhD

Associate Professor
Pharmaceutical Sciences and Exp. Therapeutics

Office: S425 PHAR
Office Phone: 319-335-8157

Lab: S453 PHAR
319-335-7629


Lab Website: https://pharmacy.uiowa.edu/directory/person/ethan-j-anderson

Deciphering the molecular mechanisms by which inflammation, oxidative stress and metabolism intersect, with an emphasis on mitochondrial physiology.

The broad focus of my research program as an independent investigator has been on deciphering the molecular mechanisms by which inflammation, oxidative stress and metabolism intersect during pathogenesis of cardiometabolic diseases. Our work is highly translational, ranging from work in cell-free systems to rodent models and scaling up to humans. One project that has been ongoing and NIH-funded since 2009 in collaboration with cardio-thoracic surgeons (R21HL098780, R01HL122863), is to determine the potential role of redox status and catecholamine metabolism in the etiology of postoperative atrial fibrillation. We collect discarded atrial tissue at time of surgery (typically CABG, valve repair/replace surgeries), and freeze a portion but also perform a variety of mitochondrial assays on the fresh myofibers. Through this project, my laboratory has established a human cardiac tissue and blood repository from >1000 patients, with matching clinical records, which we make available for investigators to use upon request.

Quite recently, my group uncovered a completely unknown and unexpected role for prohibitins (PHB1, 2) as stress-induced hepatokines, responsible for a liver to heart crosstalk during sepsis. We were recently awarded an exploratory grant from the Department of Defense (PR181274, starting April 30, 2019) to support this project. Another project involves the histidyl dipeptide L-carnosine, an endogenous dipeptide that exists in mM quantities in mammalian muscle (skeletal & cardiac) and brain tissue. Our interest in this peptide stems from our prior work on the role of lipid peroxidation, and subsequent reactive carbonyl species (RCS) formed from this, in the etiology of obesity-related disorders. We have successfully shown that carnosine mitigates many cardiometabolic disorders of obesity, likely due to its potent RCS-scavenging capacity.



PubMed link

Department/Program Affiliations:
Molecular Medicine
Pharmaceutical Sciences & Experimental Therapeutics