Journal Article Summary
The article investigates the role of DNA methyltransferase 1 in regulating the expression of the enzyme 5-α reductase type 2 (SRD5A2) in the prostate as men age. SRD5A2 is important for prostate development and is often targeted in treatments for urinary issues related to benign prostatic hyperplasia. Understanding how SRD5A2 expression changes with age and inflammation is crucial, as it could influence treatment strategies for prostate-related conditions.
The researchers studied human prostate samples and found that SRD5A2 expression was absent in about one-third of benign adult prostates. They discovered that this absence is linked to hypermethylation of the SRD5A2 promoter, which is influenced by DNA methyltransferase 1 and inflammatory factors like tumor necrosis factor α. Their findings indicate that as men age, increased methylation leads to reduced SRD5A2 expression, and that inflammation can further suppress this enzyme. Importantly, they noted that treatments targeting inflammation could potentially reactivate SRD5A2 expression.
However, the study has limitations, including the need for further research to confirm these findings in larger and more diverse populations. Patients should be aware that the expression of SRD5A2 can vary significantly, which may affect treatment outcomes for prostate conditions. It is advisable for individuals to discuss these findings with their healthcare providers, especially if they are experiencing urinary issues or considering treatments that involve SRD5A2.
Medical Safety Note
This journal article summary is provided for educational purposes only and is not medical advice. Always consult a licensed healthcare professional before starting, stopping, or changing any medication.
Article Cited
- Ge Rongbin, Wang Zongwei, Bechis Seth K., Otsetov Alexander G., Hua Shengyu, Wu Shulin, Wu Chin-Lee, Tabatabaei Shahin, et al.. DNA Methyl Transferase 1 Reduces Expression of SRD5A2 in the Aging Adult Prostate. The American Journal of Pathology 2015. DOI: 10.1016/j.ajpath.2014.11.020. PMID: 25700986. PMCID: PMC4348471.
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