Could TNF-antagonists be a novel treatment strategy for BPH patients?

Tumor necrosis factor (TNF) is widely recognized as a pivotal player in both systemic and local inflammatory processes. Due to the critical role this molecule has in driving both chronic and acute inflammation, it was among the earliest therapeutic targets utilized for pa-tients with autoimmune (AI) diseases. While inflamma-tion in the prostate is commonly observed, the organ has not previously been considered a target of systemic inflammation associated with some AI diseases. In pa-tients with benign prostatic hyperplasia (BPH), chronic inflammation is common, and immune cells represent a significant proportion of cells in the organ. Accumulation of inflammatory cells may be a response to an initial in-sult and/or a factor in driving BPH pathogenesis. Cer-tainly, inflammation can limit the efficacy of existing medical therapies in these patients. We previously showed that a pattern of gene expression in BPH tissues from patients who had progressed to indication-specific surgery was consistent with the changes seen in AI dis-eases. Recently, we demonstrated that patients with AI disease have an approximately 50% increase in (…)

Mitochondrial dysfunction and its role in tissue-specific cellular stress

Mitochondrial bioenergetics require the coordination of two different and independent genomes. Mutations in either genome will affect mitochondrial functionality and produce different sources of cellular stress. Depending on the kind of defect and stress, different tissues and organs will be affected, leading to diverse pathological conditions. There is no curative therapy for mitochondrial diseases, nevertheless, there are strategies described that fight the various stress forms caused by the malfunctioning organelles. Here, we will revise the main kinds of stress generated by mutations in mitochondrial genes and outline several ways of fighting this stress.