A photo of Daniel Prows.

Daniel R. Prows, PhD

  • Associate Professor, UC Department of Pediatrics



I work with mice conducting research to develop models of disease similar to those found in humans. Using mice in research can contribute valuable knowledge to our understanding of basic biological pathways and mechanisms of disease.

In my quest to discover novel genes and functions, I found a spontaneous mouse mutant. Spontaneous mutations in mice make excellent animal models for biomedical research targeted toward genetic diseases in humans. My goal is to identify the genetic and non-genetic factors underlying spontaneous eosinophilic myocarditis that could lead to early-onset heart failure and death.

My career in research has spanned more than 25 years. I have worked at Cincinnati Children’s since 2001 using traditional breeding strategies and genetic analyses in mice to find links that can be attributable to complex human diseases.


Genetic determinants of ammonia-induced acute lung injury in mice. Bein, K; Ganguly, K; Martin, TM; Concel, VJ; Brant, KA; Peter Di, YP; Upadhyay, S; Fabisiak, JP; Vuga, LJ; Kaminski, N; et al. American Journal of Physiology - Lung Cellular and Molecular Physiology. 2021; 320:L41-L62.

Heart disease in a mutant mouse model of spontaneous eosinophilic myocarditis maps to three loci. Zimmermann, N; Jr, GW J; Homan, SM; Prows, DR. BMC Genomics. 2019; 20.

Gpr63 is a modifier of microcephaly in Ttc21b mouse mutants. Snedeker, J; Jr, GW J; Paulding, DF; Abdelhamed, Z; Prows, DR; Stottmann, RW. PLoS Genetics. 2019; 15.

Characterization of a mouse model of hypereosinophilia-associated heart disease. Prows, DR; Klingler, A; Jr, GW J; Homan, SM; Zimmermann, N. American Journal of Physiology - Heart and Circulatory Physiology. 2019; 317:H405-H414.