Jie Peng

CD8⁺ T cells are the core effector cells of antitumor immunity. However, their functionality is vulnerable to metabolic stress within the tumor microenvironment (TME), and they experience significant inhibition from immunosuppressive signals, such as PD-1/PD-L1 and myeloid-derived suppressor cells (MDSC). This review explores how exercise enhances CD8⁺ T-cell antitumor efficacy through multidimensional synergistic mechanisms. At the molecular level, exercise stimulates the IL-15/IL-15Rα signaling pathway and triggers the release of myokines such as IL-6 and IL-7. These changes considerably boost CD8⁺ T-cell proliferation, viability, and granzyme B-dependent tumoricidal activity. Concurrently, exercise improves metabolic adaptation and sustains antitumor effects via metabolic reprogramming, which involves enhancing mitochondrial oxidative phosphorylation and increasing lactate-mediated stemness. Moreover, exercise optimizes TME vascular structure, downregulates PD-L1 expression, reduces MDSC proportion, and transforms the immunosuppressive environment, thus facilitating CD8⁺ T-cell infiltration and long-term function. Preclinical studies have verified that exercise works in tandem with immune checkpoint inhibitors, like anti-PD-1, to improve T-cell homing and counteract the depletion phenotype through the CXCR3-CXCL9/10 axis. Despite the positive progress, the mechanisms of exercise intensity, individual heterogeneity, and dynamic regulation of TME need to be explored in depth. Future studies need to combine multi-omics and dynamic immune monitoring to develop personalized exercise interventions based on CD8⁺ T-cell profiles. Exercise provides a low-cost, low-risk adjuvant strategy for cancer immunotherapy by targeting CD8⁺ T-cell function and TME remodeling, and its clinical translational potential needs large-scale validation.

Arthritis, an acute inflammatory disease affecting single or multiple joints, causes irreversible damage to cartilage and bone, leading to substantial pain and economic burden. Current treatments lack specificity. Curcumin, with its anti-inflammatory and antioxidant properties, shows promise in arthritis treatment, yet its poor water solubility and low bioavailability hinder clinical use. This study investigates the efficacy of a nanocarrier-based curcumin delivery system for non-infectious arthritis. Four types of nanocarriers-liposomes, biomolecule-based nanoparticles, nanoemulsions, and improved nanocarriers-are reviewed for their ability to target curcumin delivery. These nanocarriers improve curcumin’s therapeutic effects by enhancing pharmacokinetics, prolonging circulation, and protecting against degradation. Demonstrating potential in various non-infectious arthritis types, including ankylosing spondylitis, rheumatoid arthritis, juvenile idiopathic arthritis, and gout, this study underscores the efficacy of nanocarrier-based curcumin delivery systems in reducing inflammation, modulating immune responses, and alleviating disease symptoms. Future research should focus on optimizing nanocarrier design for increased bioavailability and conducting more clinical trials to validate safety and effectiveness in humans. Graphical abstract

Protein lipidation and ubiquitination are two fundamental post-translational modifications that orchestrate protein localization, stability, and function. Beyond their independent roles, emerging evidence reveals a complex crosstalk between these modifications that profoundly shapes tumor biology. Lipidation promotes membrane anchorage and functional activation of key oncogenic drivers, whereas ubiquitination dynamically controls protein abundance through proteasomal degradation or signaling modulation. Their interplay regulates pivotal processes in cancer, including immune evasion, tumor microenvironment remodeling, metabolic reprogramming, invasion and metastasis, and uncontrolled proliferation. Mechanistically, lipidation can shield proteins from ubiquitin-mediated degradation or recruit deubiquitinases, while ubiquitination governs the turnover and activity of lipidation enzymes, together forming a dynamic antagonistic-synergistic network. Recent advances highlight the therapeutic promise of targeting this axis: inhibitors of NMTs, DHHC enzymes, and lipidation-dependent pathways, as well as ubiquitin-based technologies such as PROTACs, DUB inhibitors, and molecular glues, are being developed toward clinical translation. By integrating mechanistic insights with therapeutic innovation, this review underscores lipidation-ubiquitination crosstalk as a critical regulatory hub and potential dual-modification target for precision oncology.

Sarcopenia and muscle atrophy are major health challenges associated with aging and various pathologies, characterized by progressive loss of muscle mass and function.

Autophagy is a vital pathway for recycling and degrading intracellular materials, closely linked to tumorigenesis and progression. The ubiquitin-specific protease (USP) family, as a critical group of deubiquitinating enzymes, plays a complex part in regulating autophagy, metabolism, immune responses, and tumor cells’ resistance to drugs. By modifying autophagy-associated proteins through deubiquitination, the USP family influences tumor cell proliferation, survival, and metabolism. Additionally, these enzymes are involved in modulating immune responses within the tumor microenvironment, thereby impacting tumor immune escape. Regarding drug resistance, the USP family enhances the tolerance of tumor cells to chemotherapeutic agents by promoting autophagy. Therefore, targeting USP family members and their regulated autophagy processes may offer new avenues for cancer therapy. This review examines the function of the USP family in tumor autophagy regulation and its implications for tumor progression. The goal of future studies should be to clarify the molecular mechanisms underlying USP-autophagy interactions and their specific roles in various tumor types to establish a theoretical framework for developing novel cancer therapeutic strategies.

The DNA cross-link repair 1B (DCLRE1B) gene is involved in repairing cross-links between DNA strands, including those associated with Hoyeraal–Hreidarsson syndrome and congenital dyskeratosis. However, its role in tumours is not well understood. DCLRE1B expression profiles were examined in tumour tissues and normal tissues using TCGA, GTEx, and TARGET datasets. Additionally, we performed experiments with clinical melanoma samples to verify DCLRE1B expression patterns. We also performed pancancer analyses to investigate the diverse roles of DCLRE1B in the biological functions of various cancers. DCLRE1B exhibited distinct expression patterns and played crucial prognostic roles in most tumours. In particular, high expression of DCLRE1B in melanoma was significantly correlated with a poor prognosis and increased malignancy. DCLRE1B was also found to be associated with the immune landscape and various immune biomarkers and regulators. Furthermore, our analysis identified potential small molecules that could target DCLRE1B in different cancer types. The DCLRE1B gene may be involved in the development and occurrence of a variety of cancers. Additionally, DCLRE1B affects various tumour types not only by mediating DNA repair but also by shaping the differential immune microenvironment. In conclusion, our research offers fresh perspectives on the diagnosis and treatment of different types of cancers.

In modern agriculture, Controlled environment agriculture (CEA) stands out as a contemporary production mode that leverages precise control over environmental conditions such as nutrient, temperature, light, and other factors to achieve efficient and high-quality agricultural production. Numerous studies have demonstrated the efficacy of manipulating these environmental factors in the short period before harvest to enhance crop yield and quality in CEA. This comprehensive review aims to provide insight into various pre-harvest practices employed in CEA, including nutrient deprivation, nutrient supply, manipulation of the light environment, and the application of exogenous hormones, with the objective of improving yield and quality in horticultural crops. Additionally, we propose an intelligent pre-harvest management system to cultivate high-quality horticultural crops. This system integrates sensor technology, data analysis, and intelligent control, enabling the customization of specific pre-harvest strategies based on producers’ requirements. The envisioned pre-harvest intelligent system holds the potential to enhance crop quality, increase yield, reduce resource wastage, and offer innovative ideas and technical support for the sustainable development of CEA.

Exercise can prevent and treat chronic diseases such as cardiovascular diseases and osteoarthritis, which are common among elderly people in rural areas.2 To further explore the practical application and socioeconomic benefits of an ‘exercise promotes health’ strategy in underdeveloped rural areas, we conducted a door-to-door survey on the exercise status and medical expenses of elderly people living in these regions. The results showed that there is a general lack of guidance and services for physical activity and exercise rehabilitation in underdeveloped rural areas, leading to low levels of awareness and poor compliance with exercise instruction and participation among elderly people. Additionally, due to limited economic resources in rural areas, equipment for the rehabilitation of elderly people is lacking. Coupled with a dearth of professional guidance from physical therapists, the disabled population often experiences slow recovery times, poor prognoses and a resultant lower quality of life.

Anemia is common in patients with rheumatoid arthritis (RA), and it is unknown whether the dietary inflammatory index (DII) is linked to anemia. This study aimed to clarify the prevalence of anemia in RA patients and its association with the DII. The data utilized in this study were collected from the National Health and Nutrition Examination Survey database from 1999 to 2018. The prevalence of anemia in RA patients was estimated by ethnicity, sex, and age. Weighted multivariate logistic regression was utilized to explore the correlation between anemia risk and DII. The most crucial dietary factors related to the risk of anemia in RA patients were screened by stepwise regression. A nomogram model was established according to key dietary factors. A total of 10.25% (confidence interval, 8.58–11.92%) of RA patients will develop anemia, with the lowest prevalence around the age of 60. In addition, higher DII levels were discovered in anemic patients than in nonanemic patients. In multivariate regression models, an important positive association was revealed between anemia and growing quartiles of DII (Q4 vs Q1: odds ratio = 1.98; confidence interval, 1.25–3.15). In the subgroup analysis, the adjusted relation of DII with anemia in females, Mexicans, smokers, nondrinkers, and age groups ≥ 60 years was statistically significant. The same association was observed in the sensitivity analysis. A nomogram model based on stepwise regression screening of key dietary factors showed good discriminatory power to identify anemic risk in RA patients (area under the curve: 0.707). In patients with RA, high DII levels were associated with the risk of anemia. More attention should be given to controlling dietary inflammation to better prevent and treat anemia.