Crosstalk between mitochondrial dysfunction and benign prostatic hyperplasia: unraveling the intrinsic mechanisms

Benign prostatic hyperplasia (BPH) represents a prevalent etiology of lower urinary tract symptoms (LUTS) in the male population, clinically defined by a non-malignant proliferation of prostatic tissue. While BPH exhibits a high prevalence among older male populations globally, the precise underlying mechanisms contributing to its development remain incompletely elucidated. Mitochondria, essential organelles within eukaryotic cells, are critical for cellular bioenergetics, the regulation of reactive oxygen species (ROS) generation, and the modulation of cell death pathways. The maintenance of mitochondrial homeostasis involves a complex interplay of processes. By synthesizing previous literature, this review discusses mitochondrial homeostasis in prostate glands and the role of mitochondrial dysfunction in the context of BPH. Furthermore, the review delved into each dimension of mitochondrial dysfunction in the specific etiology of BPH, highlighting its impact on cell survival, apoptosis, ferroptosis, oxidative stress and androgen receptor (AR). Overall, this review aims to unveil the crosstalk between mitochondrial dysfunction and BPH and identify intrinsic mechanisms.