Gene therapy for erectile dysfunction

被引:16
作者
Kendirci, M [1 ]
Gur, S [1 ]
Sikka, SC [1 ]
机构
[1] Tulane Univ, Ctr Hlth Sci, Dept Urol, Sect Androl, New Orleans, LA 70112 USA
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2005年 / 10卷
关键词
penis; erection; gene therapy; erectile dysfunction; nitric oxide; diabetes mellitus; aging;
D O I
10.2741/1733
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The past decade has seen an explosion of new information on the physiology of penile erection, pathophysiology of erectile dysfunction (ED), and development of new oral agents (e.g., three PDE5 inhibitors) to manage ED. Although all three selective PDE5 inhibitors are effective in the majority of ED cases, these oral medications have failed in certain disease states, such as diabetic ED, postprostatectomy ED, and severe veno-occlusive dysfunction. Only about 50% to 60% of these cases benefit from PDE5 inhibitor therapy, prompting the development of new approaches, including gene-based therapies for the treatment of ED. The penis is a convenient tissue target for gene therapy because of its external location and accessibility, the ubiquity of endothelial lined spaces, and low level of blood flow, especially in the flaccid state. Initially, gene therapy has been reserved for the treatment of life-threatening disorders including cancer, hereditary and acquired diseases. However, gene therapy is an attractive therapeutic possibility for the treatment of ED. Evolution of nitric oxide (NO), a small gaseous, lipophilic signaling molecule that is produced by nitric oxide synthase (NOS) activates guanylate cyclase (GC), resulting in increased cyclic guanosine monophosphate (cGMP) production, plays a significant role in our understanding of cavernosal smooth muscle physiology. Many gene therapy strategies have focused on the NO/GS/cGMP pathway. All three NOS isoforms, endothelial NOS (eNOS), neuronal NOS (nNOS), and iNOS have been used for gene therapy in order to modulate erectile response. Various viral and nonviral vectors have been used to date for the transfer of genetic material to the target cell or tissues with various degrees of success. Recently, second generation or "gutless" (helper-dependent) adenovirus vectors have been developed in order to reduce cellular toxicity and immune response, while increasing efficient gene therapy. Varieties of other gene therapy trials have also been undertaken for the treatment of ED and are the focus of this review.
引用
收藏
页码:2758 / 2769
页数:12
相关论文
共 100 条
[1]  
Andersson KE, 2001, PHARMACOL REV, V53, P417
[2]  
[Anonymous], 1992, NIH CONSENS STATEMEN, V10, P1
[3]  
Aytac IA, 1999, BJU INT, V84, P50
[4]   ENDOTHELIUM-DERIVED NITRIC-OXIDE AND CYCLOOXYGENASE PRODUCTS MODULATE CORPUS CAVERNOSUM SMOOTH-MUSCLE TONE [J].
AZADZOI, KM ;
KIM, N ;
BROWN, ML ;
GOLDSTEIN, I ;
COHEN, RA ;
DETEJADA, IS .
JOURNAL OF UROLOGY, 1992, 147 (01) :220-225
[5]   The effect of adeno-associated virus mediated brain derived neurotrophic factor in an animal model of neurogenic impotence [J].
Bakircioglu, ME ;
Lin, CS ;
Fan, PD ;
Sievert, KD ;
Kan, YW ;
Lue, TF .
JOURNAL OF UROLOGY, 2001, 165 (06) :2103-2109
[6]   Biological barriers to cellular delivery of lipid-based DNA carriers [J].
Bally, MB ;
Harvie, P ;
Wong, FMP ;
Kong, S ;
Wasan, EK ;
Reimer, DL .
ADVANCED DRUG DELIVERY REVIEWS, 1999, 38 (03) :291-315
[7]   PURIFICATION OF A NEW NEUROTROPHIC FACTOR FROM MAMMALIAN BRAIN [J].
BARDE, YA ;
EDGAR, D ;
THOENEN, H .
EMBO JOURNAL, 1982, 1 (05) :549-553
[8]  
Beckman JS, 1996, AM J PHYSIOL-CELL PH, V271, pC1424
[9]   Adenoviral gene transfer of endothelial nitric oxide synthase (eNOS) to the penis improves age-related erectile dysfunction in the rat [J].
Bivalacqua, TJ ;
Champion, HC ;
Mehta, YS ;
Abdel-Mageed, AB ;
Sikka, SC ;
Ignarro, LJ ;
Kadowitz, PJ ;
Hellstrom, WJG .
INTERNATIONAL JOURNAL OF IMPOTENCE RESEARCH, 2000, 12 (Suppl 3) :S8-S17
[10]   RhoA/Rho-kinase suppresses endothelial nitric oxide synthase in the penis: A mechanism for diabetes-associated erectile dysfunction [J].
Bivalacqua, TJ ;
Champion, HC ;
Usta, MF ;
Cellek, S ;
Chitaley, K ;
Webb, RC ;
Lewis, RL ;
Mills, TM ;
Hellstrom, WJG ;
Kadowitz, PJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (24) :9121-9126