Benign prostatic hyperplasia (BPH) is a common non-malignant condition in men over 50, defined by prostate enlargement that can lead to urinary symptoms. Although evidence suggests androgens are involved in BPH development, the underlying mechanisms of BPH remain elusive.

Atherosclerosis, a multifactorial chronic inflammatory disease of aging, is characterized by arterial wall inflammation, lipid accumulation, endothelial damage, and a dysregulated immune response. Atherosclerosis contributes to the development of multiple diseases and can result in multiorgan dysfunction. Emerging evidence suggests a strong association between systemic and local atherosclerosis of the prostatic artery, chronic inflammation, and BPH. However, it remains unclear whether the mechanisms driving atherosclerosis also support the development of BPH in aging men.

The low-density lipoprotein receptor-deficient (Ldlr-/-) mouse is a well-established model for studying atherosclerosis. It produces sustained hyperlipidemia and an atherosclerotic milieu that more closely mimics human dyslipidemia‑associated prostatic inflammation than does feeding C57BL/6 mice a high‑fat diet alone. However, this approach is insufficient to induce robust atherosclerosis or the full spectrum of metabolic and immune perturbations required to study BPH pathogenesis.