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Studies have demonstrated that dyslipidemia may directly disrupt intracavernosal neuroplasticity: it downregulates the intracavernosal expression of nerve growth factor (NGF) and vascular endothelial growth factor (VEGF), two core mediators of neural repair, an effect that impedes neural repair processes and reduces the regenerative capacity of nerve fibers ( Furthermore, evidence indicates that dyslipidemia is significantly associated with neural aging-related phenotypes and reduced neuroplasticity, which can further impair the function of the cavernous nerve plexus and central erectile regulatory circuits, serving as a potential indirect pathway for dyslipidemia to impair erectile function ( 7 Endocrine disorders 7.1 Low testosterone availability Numerous clinical studies indicate that dyslipidemia can affect testosterone levels through various pathways: a high-cholesterol diet can induce endoplasmic reticulum stress in the testes, thereby inhibiting the expression of steroidogenic enzymes and leading to decreased testosterone levels ( Studies have found that oxidized low-density lipoprotein (oxLDL) can inhibit testosterone synthesis in Leydig cells by affecting mitochondrial function and the p38 MAPK/COX-2 signaling pathway, thereby reducing testosterone availability and leading to ED ( Dyslipidemia may also contribute to testosterone deficiency through modulation of the gut microbiota, particularly via enrichment of testosterone-degrading species ( 7.2 Other endocrine alterations Other endocrine and metabolic alterations, including estrogen-androgen imbalance, insulin resistance, and leptin dysregulation, may coexist in patients with dyslipidemia
