The pathological growth of the prostate gland in atherogenic contexts

The human prostate is an androgen-dependent gland where an imbalance in cell proliferation can lead to benign prostatic hyperplasia (BPH), which results in voiding lower urinary tract symptoms in the elderly. In the last decades, novel evidence has suggested that BPH might represent an element into the wide spectrum of disorders conforming the Metabolic Syndrome (MS). The dyslipidemic state and the other atherogenic factors of the MS have been shown to induce, maintain and/or aggravate the pathological growth of different organs, with data regarding the prostate being still limited. We here review the available epidemiological and experimental studies about the association of BPH with dyslipidemias. In particular, we have focused on Oxidized Low-Density Lipoproteins (OxLDL) as a potential trigger for vascular disease and cellular proliferation in atherogenic contexts, analyzing their putative molecular mechanisms, including the induction of specific extracellular vesicles (EVs)-derived miRNAs. In addition to the epidemiological evidence, OxLDL is proposed to play a fundamental role in the upregulation of prostatic cell proliferation by activating the Rho/Akt/p27Kip1 pathway in atherogenic contexts. miR-21, miR-141, miR-143, miR-145, miR-155, and miR-221 would be involved in the transcription of genes related to the proliferative process. Although much remains to be investigated regarding the impact of OxLDL, its receptors, and molecular mechanisms on the prostate, it is clear that EVs and miRNAs represent a promising target for proliferative pathologies of the prostate gland. •OxLDL plays a fundamental role in the upregulation of prostatic cell proliferation.•OxLDL activates the Rho/Akt/p27Kip1 pathway.•Specific EV-derived miRNAs are involved in the cellular proliferative process.•EVs and miRNAs are promising targets to study anti-OxLDL approaches.