Christine Maric, PhD, FAHA, FASN

Assistant Professor
Division of Endocrinology
Department of Medicine
Georgetown University Medical Center
396 Building D
4000 Reservoir Road, NW
Washington, DC 20057 
Phone: 202 687 -5363
Fax: 202 687 -7278

Research Interests

Sex differences in diabetic renal disease.

Research Summary

There is ample evidence implicating gender as a risk factor for the impact and progression of cardiovascular and renal disease, with the incidence of these diseases being more prevalent in males than females. However, unlike most progressive diseases, in which the female gender is a protective factor, this “female advantage” appears to be lost in diabetes; the incidence of diabetes and its complications, such as diabetic nephropathy is equal and, according to some reports, even exceeds that in men. Our studies will explore some of these actions in an experimental model of diabetic nephropathy. More specifically, our studies will examine how the renin-angiotensin system, in concert with ovarian hormones, mediates structural and functional changes in diabetic animals with renal complications, i.e. diabetic nephropathy.

Representative Publications

  • Maric C, Aldred GP, Antoine AM, Dean RG, Eitle E, Mendelsohn FAO, Williams DA, Harris PJ, Alcorn D. Effects of angiotensin II on cultured rat renomedullary interstitial cells are mediated by AT1A receptors. Am J Physiol 1996; 271: F1020-F1028.
  • Maric C, Aldred GP, Harris PJ, Alcorn D. Angiotensin II inhibits growth of cultured embryonic renomedullary interstitial cells through the AT2 receptor. Kidney Int 1998; 53: 92–99.
  • Maric C, Lin P, Walther T. Neutral endopeptidase deficiency abolishes growth stimulatory properties of Ang II in renal interstitial fibroblasts. Matrix Biology (submitted Feb. 28th 2003).
  • Maric C, Sandberg K, Hinojosa-Laborde C. Age-related renal injury is ameliorated with estrogen replacement. (submitted Am J Pathol)
  • Wu Z, Maric C, Zheng W, Sandberg K. Estrogen inhibits adrenal angiotensin AT1 receptor expression by posttranscriptional mechanisms involving translational inhibition. Endocrinology (in revision 2003).