Hepatocellular carcinoma (HCC) is a leading cause of cancer-related deaths worldwide, with limited treatment options for advanced stages. Metabolic reprogramming is a hallmark of cancer, enabling tumor cells to adapt to the harsh tumor microenvironment (TME) and evade immune surveillance. This review involves the role of metabolic reprogramming in HCC, focusing on the dysregulation of glucose, lipid, and amino acid metabolism, and its impact on immune evasion. Key metabolic pathways, such as the Warburg effect, fatty acid synthesis, and glutaminolysis, are discussed, along with their influence on tumor-associated macrophages (TAMs) and immune cell function. Targeting these metabolic alterations presents a promising therapeutic approach to enhance immunotherapy efficacy and improve HCC patient outcomes.

Abnormal lipid accumulation is a fundamental contributor to obesity and metabolic disorders. Lipid droplets (LDs) and mitochondria (MT) serve as organelle chaperones in lipid metabolism and energy balance. LDs play a crucial role in lipid storage and mobilization, working in conjunction with MT to regulate lipid metabolism within the liver, brown adipose tissue, and skeletal muscle, thereby maintaining metabolic homeostasis. The novelty of our review is the comprehensive description of LD and MT interaction mechanisms. We also focus on the current drugs that target this metabolism, which provide novel approaches for obesity and related metabolism disorder treatment.

Mobile Phone Addiction represents an emergent addictive disorder that gravely jeopardizes the physical and mental health of adolescents worldwide, necessitating exhaustive research. Current reviews of MPA are in dire need of updates and enhancements. Therefore, this review aggregates the extant research spanning the past two decades on the prevalence, pathogenesis, comorbidities, assessment, and treatment of MPA, aiming to furnish a reference for future investigations into this condition.

Background: Previous research indicates that per- and polyfluoroalkyl substances (PFAS) can disrupt metabolism and neurological function via endocrine pathway interference and neuroinflammation. These effects may impair melatonin secretion and disrupt circadian rhythm regulation, suggesting potential links to sleep health. However, the impact of PFAS exposure on adolescent sleep remains unclear. This study examines the associations between PFAS exposure and sleep health indicators in U.S. adolescents.Methods: Data from 838 adolescents who participated in the 2005–2018 National Health and Nutrition Examination Survey (NHANES) were analyzed to investigate the association between PFAS exposure and physician-diagnosed sleep disorders. Eight PFAS compounds were identified. Multivariate logistic regression models, restricted cubic spline (RCS) curves, Bayesian kernel machine regression (BKMR), and weighted quantile sum (WQS) regression were used to assess single, linear, and combined effects on adolescent sleep disorders.Results: Negative associations were observed between adolescent sleep disorders and three PFAS compounds, specifically perfluorooctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS), and perfluorononanoic acid (PFNA). RCS analysis revealed a significant linear relationship (P for non-linear > 0.05). The BKMR and WQS models demonstrated a combined effect of PFAS exposure on sleep disorders, with PFOS demonstrating the most substantial contribution (effect size: 0.91). The stratified analysis revealed that PFOS exposure had a greater impact on females [odds ratio (OR): 0.54, 95% confidence interval (CI): 0.33–0.87] than males (OR: 0.50, 95% CI: 0.24–1.01), suggesting sex-specific differences in vulnerability.Conclusions: Our findings indicate a negative correlation between specific PFAS and specific sleep disorders in adolescents, with PFOS being the dominant effect component in the PFAS mixture and stronger effects observed in females. However, due to the cross-sectional nature of the study, a causal relationship cannot be established. These results highlight the potential public health impact of PFAS exposure and the need to further investigate the underlying mechanisms and causal pathways in future longitudinal or experimental studies.

Autoimmune diseases (AID) comprise a diverse group of disorders driven by aberrant B-cell and T-cell reactivity against self-tissues. In recent years, cell-based therapies utilizing engineered T cells have emerged as a promising therapeutic strategy for AIDs. Notably, chimeric antigen receptor (CAR)-T cells have demonstrated the ability to selectively target and eliminate autoreactive immune populations, including pathogenic B cells and antibody-producing plasma cells. Beyond T-cell modulation, macrophages (MΦs) exhibit remarkable plasticity, differentiating into pro-inflammatory (M1) or anti-inflammatory (M2) phenotypes in response to microenvironmental cues. Advances in genetic engineering have enabled the development of CAR-MΦs (CAR-M), which hold potential for adoptive immunotherapy in certain diseases. However, CAR-M therapy remains experimental and requires further clinical validation. This review systematically evaluates the therapeutic potential of CAR-T and CAR-M in AIDs, comparing their respective advantages and limitations to provide a comprehensive foundation for future translational applications.