Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a common and non-lethal urological condition with painful symptoms. The complexity of CP/CPPS’s pathogenesis and lack of efficient etiological diagnosis results in incomplete treatment and recurrent episodes, causing long-term mental and psychological suffering in patients. Recent findings indicate that the autonomic nervous system involves in CP/CPPS, including sensory, sympathetic, parasympathetic, and central nervous systems. Neuro-inflammation and sensitization of sensory nerves lead to persistent inflammation and pain. Sympathetic and parasympathetic alterations affect the cardiovascular and reproductive systems and the development of prostatitis. Central sensitization lowers pain thresholds and increases pelvic pain perception in chronic prostatitis. Therefore, this review summarized the detailed processes and mechanisms of the critical role of the autonomic nervous system in developing CP/CPPS. Furthermore, it describes the neurologically relevant substances and channels or receptors involved in this process, which provides new perspectives for new therapeutic approaches to CP/CPPS.

Prostatitis is a common urological condition that affects almost half of all men at some point in their life. The prostate gland has a dense nerve supply that contributes to the production of fluid to nourish sperm and the mechanism to switch between urination and ejaculation. Prostatitis can cause frequent urination, pelvic pain, and even infertility. Long-term prostatitis increases the risk of prostate cancer and benign prostate hyperplasia. Chronic non-bacterial prostatitis presents a complex pathogenesis, which has challenged medical research. Experimental studies of prostatitis require appropriate preclinical models. This review aimed to summarize and compare preclinical models of prostatitis based on their methods, success rate, evaluation, and range of application. The objective of this study is to provide a comprehensive understanding of prostatitis and advance basic research.

Background: MicroRNA(miR)-200c-3p is a tumor suppressor that helps inhibit the progression of various types of cancer. However, its role in kidney renal clear cell carcinoma (KRIC) is unknown. The purpose of this study was to explore the biological function and regulatory mechanism of miR-200c-3p in the development of KRIC.Methods: The relative levels of miR-200c-3p and vascular endothelial growth factor A (VEGFA) in KIRC tissues and cells were determined using the qRT-PCR technique. Transwell and wound healing assay methods were used to understand the effect of miR-200c-3p on the migration and invasion of 786-O and Caki-1 cells. The ability of miR-200c-3p to target VEGFA was determined using the Dual-Luciferase reporter assay system Results: MiR-200c-3p was downregulated in KIRC tissues and cell lines. The overexpression of miR-200c-3p attenuated the migratory capacities of 786-O and Caki-1 cells. The migratory ability increased under conditions of miR-200c-3p knockdown. Analysis of the results obtained using the wound healing assay revealed that overexpression of miR-200c-3p reduced the migratory abilities of Caki-1 and 786-O cells, and inhibition of miR-200c-3p accelerated the process of wound closure. Analysis of the results obtained from screening tests and by conducting the Dual-Luciferase reporter assay revealed that VEGFA was the direct target of miR-200c-3p. The VEGFA mRNA level was low in the 786-O and Caki-1 cells under conditions of overexpressed miR-200c-3p. High levels of VEGFA mRNA were observed in the cells post miR-200c-3p knockdon.Conclusions: The tumor suppression ability of miR-200c-3p in KIRC can be achieved by regulating the expression of VEGFA.