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Int J Mol Sci. 2016 Aug 11;17(8). pii: E1311. doi: 10.3390/ijms17081311.

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

Author information

1
Department of Clinical and Experimental Medicine, University of Messina, Azienda Ospedaliera Universitaria Policlinico "G. Martino", 98125 Messina, Italy. lminutoli@unime.it.
2
Department of Clinical and Experimental Medicine, University of Messina, Azienda Ospedaliera Universitaria Policlinico "G. Martino", 98125 Messina, Italy. mrinaldi@unime.it.
3
Department of Clinical and Experimental Medicine, University of Messina, Azienda Ospedaliera Universitaria Policlinico "G. Martino", 98125 Messina, Italy. hrmarini@unime.it.
4
Department of Clinical and Experimental Medicine, University of Messina, Azienda Ospedaliera Universitaria Policlinico "G. Martino", 98125 Messina, Italy. nirrera@unime.it.
5
Department of Human Pathology, University of Messina, Azienda Ospedaliera Universitaria Policlinico "G. Martino", 98125 Messina, Italy. giovanni.crea@unime.it.
6
Department of Human Pathology, University of Messina, Azienda Ospedaliera Universitaria Policlinico "G. Martino", 98125 Messina, Italy. cesare.lorenzini@unime.it.
7
Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, 98125 Messina, Italy. puzzolo@unime.it.
8
Department of Clinical and Experimental Medicine, University of Messina, Azienda Ospedaliera Universitaria Policlinico "G. Martino", 98125 Messina, Italy. andrea.valenti@unime.it.
9
Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, 98125 Messina, Italy. apisani@unime.it.
10
Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, 98125 Messina, Italy. elenabianca.adamo@unime.it.
11
Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, 98125 Messina, Italy. daltavilla@unime.it.
12
Department of Clinical and Experimental Medicine, University of Messina, Azienda Ospedaliera Universitaria Policlinico "G. Martino", 98125 Messina, Italy. fsquadrito@unime.it.
13
Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, 98125 Messina, Italy. amicali@unime.it.

Abstract

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.

KEYWORDS:

apoptosis; benign prostatic hyperplasia; treatment

PMID:
27529214
PMCID:
PMC5000708
DOI:
10.3390/ijms17081311
[Indexed for MEDLINE]
Free PMC Article

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