Macrophage dynamics in prostate cancer: Molecular to therapeutic insights.

This review provides an in-depth examination of the role that tumor-associated macrophages (TAMs) play in the progression of prostate cancer (PCa), with a particular focus on the factors influencing the polarization of M1 and M2 macrophages and the implications of targeting these cells for cancer progression. The development and prognosis of PCa are significantly influenced by the behavior of macrophages within the tumor microenvironment. M1 macrophages typically exhibit anti-tumor properties by secreting pro-inflammatory cytokines such as interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α), thereby enhancing the immune response. Conversely, M2 macrophages contribute to tumor cell migration and invasion through the production of factors like arginase-1 (Arg1) and interleukin-10 (IL-10). This review not only explores the diverse factors that affect macrophage polarization but also delves into the potential therapeutic strategies targeting macrophage polarization, including the critical roles of non-coding RNA and exosomes in regulating this process. The polarization state of macrophages is highlighted as a key determinant in PCa progression, offering a novel perspective for clinical treatment. Future research should concentrate on gaining a deeper understanding of the molecular mechanisms underlying macrophage polarization and on developing effective targeted therapeutic strategies. The exploration of the potential of combination therapies to improve treatment efficacy is also emphasized. By emphasizing the importance of macrophages as a therapeutic target in PCa, this review aims to provide valuable insights and research directions for clinicians and researchers.

LncRNA SNHG1 serves as a biomarker for systemic lupus erythematosus and participates in the disease progression.

LncRNAs play an important role in autoimmune diseases. The purpose of this study was to explore the role of lncRNA SNHG1 in systemic lupus erythematosus (SLE), and laid a theoretical foundation for the study of SLE. The basic clinical information of all subjects was first collected for statistical analysis, and SNHG1 expression in the serum of all subjects was detected by RT-qPCR. The value of SNHG1 in the diagnosis of SLE was assessed by ROC. The correlation between SNHG1 and each blood sample index was analyzed by Pearson correlation analysis. The role of SNHG1 in primary peripheral blood mononuclear cells (PBMCs) apoptosis was explored. SNHG1 expression is relatively upregulated in patients with SLE compared to healthy people. SNHG1 expression was positively correlated with SLEDAI score, IgG, CRP, and ESR, and negatively correlated with C3 and C4. ROC indicated that SNHG1 has the potential to assist in the diagnosis of SLE. PBMCs apoptosis in SLE was higher than that in control group, the knockdown and overexpression of SNHG1 could correspondingly inhibit and promote PBMCs apoptosis. SNHG1 has the potential to be a diagnosis marker for SLE and may be involved in regulating PBMCs apoptosis.

Homocysteine, interleukin-1ß, and fasting blood glucose levels as prognostic markers for diabetes mellitus complicated with cerebral infarction and correlated with carotid intima-media thickness.

Diabetes mellitus complicated with cerebral infarction (DMCI) has a high incidence and disability rate. Therefore, identification of biomarkers for the early prediction of the development and progression of cerebral infarction (CI) is of great significance for the prevention and treatment of this disease. The roles of serum homocysteine (Hey), interleukin-1ß (IL-1ß), and fasting blood glucose (FBG) in DMCI and their correlations with carotid intima-media thickness (CIMT) were explored. A total of 124 patients with DMCI (DMCI group) and 103 patients with diabetes mellitus (DM) (DM group) admitted to the People's Hospital of Liuhe District of Nanjing were enrolled in this study. A further 100 healthy controls undergoing physical examinations during the same period (HC group) were also enrolled. CIMT value was detected by carotid artery ultrasound. Hey and FBG levels were determined by a fully automatic biochemical analyzer. The IL-1ß level was detected by enzyme-linked immunosorbent assay (ELISA). The levels of Hey, IL-1ß, and FBG and the CIMT value in the DMCI and DM groups were significantly higher than those in the HC group (P<0.001). The levels and the value in the DMCI group were significantly higher than those in the DM group (P<0.001). Hey, IL-1ß, and FBG levels were positively correlated with CIMT value (r=0.542, P<0.001; r=0.522, P<0.001; r=0.402, P<0.001). Receiver operating characteristic (ROC) curves showed that the sensitivity and specificity of Hey for diagnosing DMCI were 86.29 and 80.58%; those of IL-1ß were 68.55 and 86.41%; those of FBG were 69.35 and 88.35%. Multivariate logistic regression analysis revealed that systolic blood pressure (SBP), diastolic blood pressure (DBP), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), Hey, IL-1ß, FBG, and CIMT were independent risk factors for DMCI (P<0.05). In conclusion, patients with DMCI have severe atherosclerosis. Hey, IL-1ß, and FBG are involved in the development and progression of DMCI, so they can be used as predictive markers for the disease. Hey, IL-1ß, FBG, and CIMT are independent risk factors for patients with DMCI.