Klimecki, Walter

Office Location:

Pharmacy 314

Skaggs College of Pharmacy

1703 E Mabel

Tucson AZ 85721


Primary Phone: (520) 6267470
Email: klimecki@pharmacy.arizona.edu
Website: http://www.pharmacy.arizona.edu/directory/walter-klimecki-dvm-phd
Education:

Ph.D., Pharmacology and Toxicology, University of Arizona, 1994

D.V.M., Ohio State University, 1984

 

College Affiliations:
  • College Of Medicine
  • College Of Public Health
  • College Of Pharmacy
Research Interests:

 Associating human genetic backgrounds and diverse environmental exposures to understand individual variability in disease susceptibility. Metals Toxicology, Mechanism of Action of Arsenic, Toxicity Toxicant Disruption of Cellular Metabolism

Environmental Health Research & Expertise:

Dr. Klimecki’s research spans the translational spectrum, from the use of basic experimental models of toxicology in mechanism of action studies to epidemiological studies of toxicant exposed human populations.  Dr. Klimecki’s work in human studies of arsenic-exposed populations has defined important predictors of “safer” and “less safe” arsenic bioconversion, including gender, body mass index, genetic variation in the AS3MT gene, and the degree of indigenous American ancestry.  His “bench” mechanistic toxicology studies have identified novel consequences of arsenic exposure.  Klimecki’s group was among the first to characterize autophagy, a process of cellular organelle self-catabolism , as a key process resulting from arsenite exposure to cultured cells.  More recently, his group has broken new ground in our understanding of the ability of arsenic to perturb fundamental energy metabolism in human cells.  His group demonstrated that cells, even cells that are exposed to abundant oxygen, launch an arsenic response that is more typically associated with hypoxic stress.  Part of this response is switching energy metabolism from oxidative phosphorylation to glycolysis.  This energy metabolism re-programming has important consequences on the resulting cellular phenotype and may underlie arsenic-induced human pathology.

Publications:
RFG1