Next Article in Journal
ST6GALNAC5 Expression Decreases the Interactions between Breast Cancer Cells and the Human Blood-Brain Barrier
Next Article in Special Issue
Melatonin Alleviates Liver Apoptosis in Bile Duct Ligation Young Rats
Previous Article in Journal
The Potential Role of Kallistatin in the Development of Abdominal Aortic Aneurysm
Previous Article in Special Issue
Zeb1 Is a Potential Regulator of Six2 in the Proliferation, Apoptosis and Migration of Metanephric Mesenchyme Cells
Open AccessReview

Apoptotic Pathways Linked to Endocrine System as Potential Therapeutic Targets for Benign Prostatic Hyperplasia

1
Department of Clinical and Experimental Medicine, University of Messina, Azienda Ospedaliera Universitaria Policlinico “G. Martino”, 98125 Messina, Italy
2
Department of Human Pathology, University of Messina, Azienda Ospedaliera Universitaria Policlinico “G. Martino”, 98125 Messina, Italy
3
Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, 98125 Messina, Italy
*
Author to whom correspondence should be addressed.
Academic Editor: Anthony Lemarié
Int. J. Mol. Sci. 2016, 17(8), 1311; https://doi.org/10.3390/ijms17081311
Received: 8 July 2016 / Revised: 26 July 2016 / Accepted: 4 August 2016 / Published: 11 August 2016
(This article belongs to the Collection Programmed Cell Death and Apoptosis)
Benign prostatic hyperplasia (BPH) is a chronic condition common in older men that can result in bothersome lower urinary tract symptoms. The molecular mechanisms and networks underlying the development and the progression of the disease are still far from being fully understood. BPH results from smooth muscle cell and epithelial cell proliferation, primarily within the transition zone of the prostate. Apoptosis and inflammation play important roles in the control of cell growth and in the maintenance of tissue homeostasis. Disturbances in molecular mechanisms of apoptosis machinery have been linked to BPH. Increased levels of the glycoprotein Dickkopf-related protein 3 in BPH cause an inhibition of the apoptosis machinery through a reduction in B cell lymphoma (Bcl)-2 associated X protein (Bax) expression. Inhibitors of apoptosis proteins influence cell death by direct inhibition of caspases and modulation of the transcription factor nuclear factor-κB. Current pharmacotherapy targets either the static component of BPH, including finasteride and dutasteride, or the dynamic component of BPH, including α-adrenoceptor antagonists such as tamsulosin and alfuzosin. Both these classes of drugs significantly interfere with the apoptosis machinery. Furthermore, phytotherapic supplements and new drugs may also modulate several molecular steps of apoptosis. View Full-Text
Keywords: benign prostatic hyperplasia; apoptosis; treatment benign prostatic hyperplasia; apoptosis; treatment
Show Figures

Graphical abstract

MDPI and ACS Style

Minutoli, L.; Rinaldi, M.; Marini, H.; Irrera, N.; Crea, G.; Lorenzini, C.; Puzzolo, D.; Valenti, A.; Pisani, A.; Adamo, E.B.; Altavilla, D.; Squadrito, F.; Micali, A. Apoptotic Pathways Linked to Endocrine System as Potential Therapeutic Targets for Benign Prostatic Hyperplasia. Int. J. Mol. Sci. 2016, 17, 1311.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop