Peripheral nerve injuries are a prevalent global issue that has garnered great concern. Although autografts remain the preferred clinical approach to repair, their efficacy is hampered by factors like donor scarcity. The emergence of nerve guidance conduits as novel tissue engineering tools offers a promising alternative strategy. This review aims to interpret nerve guidance conduits and their commercialization from both clinical and laboratory perspectives. To enhance comprehension of clinical situations, this article provides a comprehensive analysis of the clinical efficacy of nerve conduits approved by the United States Food and Drug Administration. It proposes that the initial six months post-transplantation is a critical window period for evaluating their efficacy. Additionally, this study conducts a systematic discussion on the research progress of laboratory conduits, focusing on biomaterials and add-on strategies as pivotal factors for nerve regeneration, as supported by the literature analysis. The clinical conduit materials and prospective optimal materials are thoroughly discussed. The add-on strategies, together with their distinct obstacles and potentials are deeply analyzed. Based on the above evaluations, the development path and manufacturing strategy for the commercialization of nerve guidance conduits are envisioned. The critical conclusion promoting commercialization is summarized as follows: 1) The optimization of biomaterials is the fundamental means; 2) The phased application of additional strategies is the emphasized direction; 3) The additive manufacturing techniques are the necessary tools. As a result, the findings of this research provide academic and clinical practitioners with valuable insights that may facilitate future commercialization endeavors of nerve guidance conduits.

The heterogeneity of head and neck squamous cell carcinoma (HNSCC) poses a significant challenge to treatment, underscoring the urgent need for more precise and personalized therapeutic approaches. CD8⁺ T cells, integral components of the tumor immune microenvironment, have emerged as key targets for immunotherapy. Our research has established a correlation between a decrease in CD8⁺ T cell score and a poor clinical prognosis, highlighting the prognostic value of this biomarker. By analyzing the gene expression related to CD8⁺ T cells, we have differentiated HNSCC into cold and hot tumor subtypes, uncovering disparities in clinical prognosis and responses to immunotherapy. Utilizing eight machine learning methods, we identified the key gene OLR1. Single-cell analysis of HNSCC tissues and peripheral blood, along with spatial transcriptome analysis, revealed that OLR1 predominantly functions in macrophages, modulating the immune microenvironment of HNSCC. The expression level of OLR1 may serve as a predictive marker for immunotherapy responses. Moreover, drug sensitivity analysis and molecular docking studies have indicated that simvastatin and pazopanib are potential inhibitors of OLR1. These findings suggest that simvastatin and pazopanib could open up innovative potential therapeutic avenues for individuals with HNSCC.

In recent decades, the limitations of therapeutic interventions have elevated neurological disorders and injuries to a prominent position in academic research. Existing neurotherapeutic methodologies have demonstrated insufficient efficacy in fostering neural regeneration. The current integration of precision medicine technologies and innovative tissue engineering methods holds significant promise for attaining neural regeneration. The cGAS–STING pathway, a pivotal component of the innate immune system, plays a crucial role in the pathological processes of various neurological diseases and injuries. In neuroinflammatory diseases and neural injuries, aberrant activation of the cGAS–STING pathway amplifies neuroinflammation, type I interferon responses, and cell death. Inhibition of cGAS–STING-related genes holds promise for promoting neural regeneration following disease recovery and defect regeneration. In this review, the foundational pathophysiological mechanisms underlying cGAS–STING-related gene regulation in neurological disorders and injuries are elucidated with a special emphasis on its implications in nerve-related cells. In this review, we highlight the advances in tissue engineering technologies that integrate cGAS–STING pathway modulators, highlighting their potential therapeutic efficacy in modulating neural regeneration. Nevertheless, the role of the cGAS–STING pathway in neural regeneration remains relatively limited. Bibliometric analysis demonstrates a significant correlation of cGAS–STING pathway activation with various neuropathological processes. Studies have progressively focused on the critical role of this pathway in neurological diseases and injuries. As it stands, the effectiveness of tissue engineering technologies involving cGAS–STING-related gene modulators in achieving neural regeneration remains unfulfilled in its potential. Future research must apply advanced omics technologies to further delineate the exact functions of the cGAS–STING pathway in neural regeneration. Integration of these results with precision medicine approaches will be necessary for creating tissue engineering biomaterials with capabilities for precise delivery and targeted controlled release of cGAS–STING-related genes in neural regeneration-related cells, towards functional recovery from neurological injury and diseases.

Background: the paucity of early diagnostic markers for clear cell renal cell carcinoma (ccRCC) contributes significantly to its poor clinical prognosis. Aberrations in fatty acid metabolism (FAM) have been implicated in the progression of this malignancy, suggesting the metabolic pathway as a potential target for novel therapeutic approaches. Results: this investigation demonstrated that FAM was decreased in ccRCC, which correlated with a worsening clinical prognosis. A prognostic signature was constructed using FAM-associated long noncoding RNAs (lncRNAs), highlighting notable differences in the tumor microenvironment and treatment responses between high- and low-risk groups. This study employed a suite of six machine learning algorithmsleast absolute shrinkage and selection operator (LASSO) regression, eXtreme gradient boosting (XGBoost), support vector machine recursive feature elimination (SVM-RFE), Random Forest, gradient boosting machine (GBM), and decision treeto identify a significant regulatory axis involving SRD5A3-AS1, hsa-let-7e-5p, and RRM2. The single-cell analysis of ccRCC tissues and peripheral blood, as well as a spatial transcriptomic analysis, revealed that this regulatory axis suppresses FAM in precursor CD8⁺ T cells. These cells exacerbate the clinical outcomes of ccRCC by affecting other immune cells through the macrophage migration inhibitory factor (MIF). Drug sensitivity assays identified axitinib and sorafenib as potential SRD5A3-AS1 inhibitors and dasatinib and fulvestrant as RRM2 inhibitors. The molecular docking results confirmed the stability of the binding of RRM2 to dasatinib and fulvestrant, suggesting that these drugs are promising for therapeutic applications in ccRCC.