One of the most common urological diseases is benign prostatic hyperplasia (BPH), with a high prevalence in the middle-aged and elderly male population. Patient's mental and physical health is affected significantly by this condition, causing them considerable discomfort. During the development of BPH, a synergistic effect occurs in response to inflammation, oxidative stress, and apoptosis induced by the activation of macrophages. The nuclear factor erythroid2-related factor 2 (Nrf2) signaling pathway can mediate macrophage activation and inhibit prostate hyperplasia by suppressing pro-inflammatory factors, anti-oxidative stress disorder, and initiating apoptosis. The purpose of this study was to review the mechanism of action of Nrf2 signaling pathway-mediated macrophage activation on the immune microenvironment of BPH and to summarize the Chinese medicine based on Nrf2 to provide an overview of BPH treatment options.

Prostate-related diseases, including prostatitis, benign prostatic hyperplasia (BPH), and prostate cancer (PCa), represent significant threats to the health of the aging male population worldwide. Despite their prevalence, the pathogenesis of prostate-related diseases has not been elucidated. Recent studies have shown that N ⁶ -methyladenosine (m ⁶ A) modification is widely involved in the progression of prostate-related diseases. In this review, we summarized recent advances in understanding the core m ⁶ A regulatory machinery comprising writers such as the methyltransferase-like 3 (METTL3)-METTL14 complex, erasers including fat mass and obesity-associated protein (FTO) and AlkB homolog 5 (ALKBH5), and readers, including the YTH domain-containing family proteins (YTHDFs), YTHDC proteins, insulin-like growth factor 2 mRNA-binding proteins (IGF2BPs), and heterogeneous nuclear ribonucleoproteins (HNRNPs). Specifically, we elucidated how dysregulation of these components drives disease progression via alterations in cellular proliferation, differentiation, inflammatory responses, and stem cell dynamics. Notably, m ⁶ A modifications help shape the immunosuppressive landscape in PCa by modulating immune checkpoint expression, cytokine networks, and immune cell infiltration, thereby critically influencing therapeutic responses to immunotherapy. Furthermore, this review highlights the emerging diagnostic potential and therapeutic viability of m ⁶ A-targeted strategies, offering valuable insights for future clinical translation in prostate-related diseases.

Diabetes mellitus comprises a group of heterogeneous metabolic disorders characterized by persistent hyperglycemia, progressive β-cell dysfunction, and multi-organ complications. Although type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) have distinct pathogenic origins, both involve immune dysregulation, tissue stress, release of danger signals, and chronic inflammation. Dendritic cells (DCs), as antigen-presenting cells, integrate innate immune sensing, antigen presentation, cytokine production, T-cell regulation, and peripheral immune tolerance, placing them at a critical interface between autoimmunity and metabolic inflammation. In T1DM, DCs contribute to β-cell autoantigen presentation, tolerance breakdown, autoreactive T-cell activation, and insulitis amplification. In T2DM, DCs may contribute to adipose tissue inflammation, hepatic immunometabolic crosstalk, β-cell stress, vascular inflammation, and immune remodeling associated with diabetes-related complications. Here, we review the disease-specific roles of DC subsets in T1DM and T2DM and discuss shared molecular mechanisms, including pattern-recognition receptor signaling, metabolic reprogramming, inflammasome activation, cytokine networks, and the shift from immune tolerance to inflammation. We also evaluate therapeutic DC reprogramming strategies and their potential implications for targeted immunometabolic intervention in diabetes.