A photo of Joshua Waxman.

Associate Professor, UC Department of Pediatrics

513-636-7232

513-636-5958

Biography & Affiliation

Biography

The main areas of my research are cardiovascular development, regeneration, molecular genetics and signaling pathways. My lab uses zebrafish as our primary research model to uncover conserved mechanisms underlying normal heart development and regeneration, and the causes of congenital cardiovascular defects.

Research from my lab has identified novel mechanisms by which the developing heart progenitors are patterned and by which differentiated cardiac cells maintain their identity. One question my lab is particularly interested in is how cardiac progenitor cells are selected, which ultimately determine the proper size of the heart.

I became interested in better understanding the molecular and genetic mechanisms of cardiovascular development and disease through my broader interests in developmental biology and organogenesis.

I have more than 20 years’ experience in the field of developmental biology and I spent more than 15 years studying cardiovascular development. I first joined the Molecular Cardiovascular Biology Division at Cincinnati Children’s Hospital Medical Center in late 2009. I have received a K99/R00 Pathway to Independence Award from the National Institutes of Health (NIH), a March of Dimes via the Basil O’Connor Starter Scholar Research Award, March of Dimes Research Grant and multiple NIH R01s to fund my research.

Research from my lab has been published in journals, including PLoS Biology, PLoS Genetics and Development.

Research Interests

Cardiac development; heart regeneration; congenital heart defects; molecular signaling pathways; transcription factors; retinoid acid signaling; zebrafish

Academic Affiliation

Associate Professor, UC Department of Pediatrics

Research Divisions

Molecular Cardiovascular Biology, Heart, Developmental Biology

Education

BA: New College, Sarasota, FL,1999.

PhD: University of Washington, Seattle, WA, 2004.

Postdoctoral Fellow: Skirball Institute/NYU School of Medicine, New York, NY, 2004-2009.

Publications

Ccdc103 promotes myeloid cell proliferation and migration independent of motile cilia. Falkenberg, LG; Beckman, SA; Ravisankar, P; Dohn, TE; Waxman, JS. DMM Disease Models and Mechanisms. 2021; 14.

Retinoic acid signaling restricts the size of the first heart field within the anterior lateral plate mesoderm. Duong, TB; Holowiecki, A; Waxman, JS. Developmental Biology. 2021; 473:119-129.

Ccdc103 promotes myeloid cell proliferation and migration independent of motile cilia. Falkenberg, LG; Beckman, SA; Ravisankar, P; Dohn, TE; Waxman, JS. DMM Disease Models and Mechanisms. 2021.

Atrial and Sinoatrial Node Development in the Zebrafish Heart. Martin, KE; Waxman, JS. Journal of Cardiovascular Development and Disease. 2021; 8.

Retinoic Acid Signaling and Heart Development. Perl, E; Waxman, JS. Sub-Cellular Biochemistry. 2020; 95:119-149.

Pbx4 limits heart size and fosters arch artery formation by partitioning second heart field progenitors and restricting proliferation. Holowiecki, A; Linstrum, K; Ravisankar, P; Chetal, K; Salomonis, N; Waxman, JS. Development (Cambridge). 2020; 147.

Pbx4 limits heart size and fosters arch artery formation through partitioning second heart field progenitors and restricting proliferation. Holowiecki, A; Linstrum, K; Ravisankar, P; Chetal, K; Salomonis, N; Waxman, JS. Development (Cambridge). 2020.

Reiterative Mechanisms of Retinoic Acid Signaling during Vertebrate Heart Development. Perl, E; Waxman, JS. Journal of Developmental Biology. 2019; 7.

HDAC1-mediated repression of the retinoic acid-responsive gene ripply3 promotes second heart field development. Song, YC; Dohn, TE; Rydeen, AB; Nechiporuk, AV; Waxman, JS. PLoS Genetics. 2019; 15.

Enhancing regeneration after acute kidney injury by promoting cellular dedifferentiation in zebrafish. Skvarca, LB; Han, HI; Espiritu, EB; Missinato, MA; Rochon, ER; McDaniels, MD; Bais, AS; Roman, BL; Waxman, JS; Watkins, SC; et al. DMM Disease Models and Mechanisms. 2019; 12.