Nestor Gonzalez-Cadavid, Ph.D.
Professor of Medicine
DNA Repository and Molecular Medicine Core Leader
Charles Drew University of Medicine and Science
1731 E. 120th Street
Los Angeles, CA 90059

Phone: (323) 563-9330
ncadavid@ucla.edu

Dr. Gonzalez-Cadavid is the Director of the RCMI Molecular Medicine Core at Charles Drew University and also supervises
a research group in the Division of Endocrinology focused on the study of the mechanisms that operate in the loss of skeletal muscle fibers (sarcopenia) during aging and some chronic pathological conditions, and in the impairment of muscle regeneration after injury or in muscle dystrophies (degeneration).

The emphasis of this research is on the role of myostatin, a growth and differentiation factor that acts as a negative regulator of skeletal muscle mass, and of anabolic androgens like testosterone, on the commitment of stem cells to different cell lineages related to the formation of muscle (myogenesis) or its pathological replacement by fibrotic (myofibroblast generation) and fat (adipogenesis) tissues. These dormant stem cells present in adult skeletal muscle are potential targets for in vivo modulation by pharmacological agents or by gene therapy using recombinant DNA, and we aim to force them to express certain genes that may help the diseased muscle to undergo myogenesis rather than fibrosis or fat infiltration.

The adult stem cells are also cultured and transformed ex vivo by gene therapy and growth factors and later transplanted
into mouse models aiming to improve muscle regeneration and prevent or regress fibrosis. Our research involves basic approaches of cell culture, molecular biology, physiology, and experimental animal work and is NIH funded.

Davila HH, Rajfer J, and Gonzalez-Cadavid NF. 2004. Corporal veno-occlusive dysfunction in aging rats: evaluation by cavernosometry and cavernosography. Urology. 64(6):1261-6.


Jalkut M, Gonzalez-Cadavid N , and Rajfer J. 2004. New discoveries in the basic science understanding of Peyronie's disease. Curr Urol Rep. 5(6):478-84.

Gonzalez-Cadavid NF and Rajfer J. 2004. Molecular pathophysiology and gene therapy of aging-related erectile dysfunction.
Exp Gerontol. 39(11-12):1705-12.

Jasuja R, Ramaraj P, Phong Mac R, Singh AB, Storer TW, Artaza J, Miller A, Singh R, Taylor WE, Lee ML, Davidson T, Sinha-Hikim I, Gonzalez-Cadavid N, and Bhasin S. 2004. Delta-4-androstene-3,17-dione (4-androstenedione) Binds Androgen Receptor, Promotes Myogenesis in Vitro, and Increases Serum Testosterone Levels, Fat-Free Mass, and Muscle Strength in Hypogonadal Men. J Clin Endocrinol Metab. Nov 2; [Epub ahead of print].

Sinha-Hikim I, Taylor WE, Gonzalez-Cadavid NF, Zheng W, and Bhasin S. 2004. Androgen receptor in human skeletal muscle and cultured muscle satellite cells: up-regulation by androgen treatment. J Clin Endocrinol Metab. 89(10):5245-55.

Qian A, Meals RA, Rajfer J, and Gonzalez- Cadavid NF. 2004. Comparison of gene expression profiles between Peyronie's disease and Dupuytren's contracture. Urology. 64(2):399-404.

Davila HH, Magee TR, Vernet D, Rajfer J, and Gonzalez- Cadavid NF. 2004. Gene transfer of inducible nitric oxide synthase complementary DNA regresses the fibrotic plaque in an animal model of Peyronie's disease. Biol Reprod. 71(5):1568-77.

Gonzalez-Cadavid NF and Bhasin S. 2004. Role of myostatin in metabolism. Curr Opin Clin Nutr Metab Care. 7(4):451-7.

Gonzalez-Cadavid NF andRajfer J. 2004. Therapy of erectile dysfunction: potential future treatments. Endocrine. 23(2-3):167-76.

Ferrini MG, Davila HH, Valente EG, Gonzalez-Cadavid NFand Rajfer J. 2004. Aging-related induction of inducible nitric oxide synthase is vasculo-protective to the arterial media. Cardiovasc Res. 61(4):796-805.

Valente EG, Vernet D, Ferrini MG, Qian A, Rajfer J, and Gonzalez-Cadavid NF. 2003. L-arginine and phosphodiesterase (PDE) inhibitors counteract fibrosis in the Peyronie's fibrotic plaque and related fibroblast cultures. Nitric Oxide. 9(4):229-44.

Liu W, Thomas SG, Asa SL, Gonzalez-Cadavid N, Bhasin S, and Ezzat S. 2003. Myostatin is a skeletal muscle target of growth hormone anabolic action. J Clin Endocrinol Metab. 88(11):5490-6.

Bhasin S, Taylor WE, Singh R, Artaza J, Sinha-Hikim I, Jasuja R, Choi H, and Gonzalez-Cadavid NF. 2003. The mechanisms of androgen effects on body composition: mesenchymal pluripotent cell as the target of androgen action. J Gerontol A Biol Sci Med Sci. 58(12):M1103-10.

Singh R, Artaza JN, Taylor WE, Gonzalez-Cadavid NF, and Bhasin S. 2003. Androgens stimulate myogenic differentiation and inhibit adipogenesis in C3H 10T1/2 pluripotent cells through an androgen receptor-mediated pathway. Endocrinology. 144(11):5081-8.

Reisz-Porszasz S, Bhasin S, Artaza JN, Shen R, Sinha-Hikim I, Hogue A, Fielder TJ, and Gonzalez-Cadavid NF. 2003. Lower skeletal muscle mass in male transgenic mice with muscle-specific overexpression of myostatin. Am J Physiol Endocrinol Metab. 285(4):E876-88.

Last updated 03/20/05