Bioengineering & Translational Medicine最新文献

Blood is a liquid connective tissue containing cellular and non-cellular components. Blood circulation is vital to life since it transports gases and nutrients, maintains immune surveillance, promotes necessary clotting to prevent hemorrhage, and maintains oncotic pressure and body temperature. Blood transfusion is a life-saving procedure where donor-derived blood is administered into a patient when the patient's own blood is diseased or depleted. However, blood transfusion faces tremendous challenges due to donor shortage, limited shelf life, transfusion-associated infection risks, and complex logistics of blood banking and transport. A robust volume of research is currently focused on resolving these issues, including pathogen reduction technologies, temperature-reduced storage, and bioreactor-based production of blood cells from stem cells in vitro. In parallel, significant interest has developed toward biomaterials-based engineering of synthetic blood surrogates that can provide critical functions of blood components while circumventing the limitations of donor-derived blood products. Here, the major efforts have focused on the design of RBC surrogates for oxygen transport and platelet surrogates for hemostatic functions, and only limited efforts have focused on WBC mimicry. Processes have also been developed to isolate plasma or coagulation factors to treat specific bleeding risks, as well as freeze-dry or spray-dry plasma for long-term storage and on-demand use. The current article will provide a comprehensive review of various blood surrogate approaches highlighting biomaterials design and applications, important challenges, and future opportunities.

This study aims to optimize the embolization endpoint to improve therapeutic outcomes in interventional procedures and minimize the risk of ectopic embolism caused by excessive embolic agent injection. Hemodynamic changes during embolization were simulated by modeling the terminal resistance vessels as a porous medium. An in vitro experimental platform has been developed to replicate the embolization process. Based on these simulations and experimental data, a quantitative method was established to evaluate the embolization endpoint using local arterial blood pressure. The method was further validated through renal artery embolization experiments in pigs. The quantitative method effectively predicted changes in local arterial pressure and flow rate, with an average error of approximately 1.65% in simulations and 3.09% in in vitro experiments. In animal studies, the pressure-based endpoint evaluation method closely aligned with imaging results, reducing the required embolic agent by an average of 17.86%. Local arterial blood pressure is considered a reliable criterion for determining the embolization endpoint, offering a relatively standardized and quantitative approach to embolization endpoint assessment. This method has significant clinical value in reducing radiation exposure and facilitating the automation of embolic agent injection procedures in the field of embolization therapy for solid tumors.

Diabetic foot ulcers (DFUs), a debilitating complication of diabetes, are exacerbated by persistent inflammation that disrupts wound repair. This study explores the therapeutic potential of antibiotic-loaded bone cement (ALBC) in modulating NLRP3 inflammasome activation and macrophage polarization to resolve chronic inflammation and accelerate healing. Using db/db diabetic mice with dorsal wounds and RAW264.7 macrophages under high-glucose conditions, we tested graded ALBC doses (high-dose ALBC, low-dose ALBC, and medium-dose ALBC) both in vivo and in vitro. Multi-modal analyses—including cytokine profiling (enzyme-linked immunosorbent assay), macrophage phenotyping (flow cytometry/immunofluorescence), and molecular pathway interrogation (reverse transcription quantitative PCR/Western blot)—revealed that ALBC dose-dependently suppressed NLRP3 inflammasome assembly, reduced IL-1β/IL-18 secretion, and skewed macrophages toward anti-inflammatory M2 phenotypes. Pharmacological NLRP3 activation reversed these effects, confirming pathway specificity. ALBC-treated wounds exhibited accelerated re-epithelialization, collagen deposition, and angiogenesis, correlating with attenuated systemic inflammation. Crucially, clinical DFU samples mirrored preclinical findings, showing NLRP3 downregulation and M2 dominance in ALBC-responsive cases. These results demonstrate that ALBC orchestrates immunometabolic reprogramming by silencing NLRP3-driven inflammation and fostering pro-reparative macrophage responses. By bridging biomaterial engineering with immunomodulation, this work advances a translatable strategy for refractory DFU management, offering a dual-action therapeutic platform that combines localized antibiotic delivery with microenvironmental immune reset.

This comprehensive review explores the therapeutic potential of carbon nanomaterials, including carbon nanotubes, graphene, carbon dots, and other related materials, in wound healing applications. These materials offer a cutting-edge approach by modulating critical cellular processes, addressing current challenges in wound care, and advancing tissue regeneration techniques. The article thoroughly examines recent developments in carbon nanomaterials, highlighting their integration into wound care strategies and the ongoing efforts to overcome limitations such as biocompatibility, toxicity, and long-term safety. Unlike previous reviews, this work not only acknowledges recent advancements but also provides a critical analysis of the still existing barriers and novel strategies for effectively translating these materials from research to clinical applications. By emphasizing both the potential and the challenges, the review aims to present a unique perspective on the future of carbon nanomaterials in wound healing, paving the way for more efficient and personalized treatment options.

Treatment of High-grade serous ovarian cancer (HGSOC) is often ineffective due to frequent late-stage diagnosis and development of resistance to therapy. Timely selection of the most effective (combination of) drug(s) for each patient would improve outcomes, however the tools currently available to clinicians are poorly suited to the task. We here present a computational simulator capable of recapitulating cell response to treatment in ovarian cancer. The technical development of the in silico framework is described, together with its validation on both cell lines and patient- derived laboratory models. A calibration procedure to identify the parameters that best recapitulate each patient's response is also presented. Our results support the use of this tool in preclinical research, to provide relevant insights into HGSOC behavior and progression. They also provide a proof of concept for its use as a personalized medicine tool and support disease monitoring and treatment selection.

Renal ischemia–reperfusion injury (IRI) is a significant condition that leads to acute kidney injury, exacerbating the progression of renal failure clinically and affecting the patient's prognosis. Following the identification of miR-182-5p as a significant molecule in IRI, we conducted a detailed analysis of its potential downstream genes and assessed its involvement in the SIRT1/Nrf2/ferroptosis pathway. To validate these findings in vivo, we implemented an exosome-mediated drug delivery protocol and assessed its therapeutic efficacy in C57BL/6. miR-182-5p exhibited a notable upregulation in renal IRI. Utilizing bioinformatics approaches, the study further investigated and validated its downstream SIRT1/Nrf2 pathway, establishing its role in ferroptosis. By employing LTHVVWL(LTH)-anchored exosomes, the delivery of miR-182-5p to the kidney was significantly improved, thereby illustrating its potential efficacy in mitigating renal IRI. The findings of our study demonstrated that miR-182-5p suppressed SIRT1/Nrf2 activity and facilitated ferroptosis, suggesting its potential as a therapeutic target for clinical IRI treatment. The inhibition of miR-182-5p via LTH-anchored exosomes was shown to significantly mitigate renal IRI, providing a novel approach for the development of miRNA-based therapeutic drug delivery systems.

The bioprinting revolution has opened new frontiers in the design and fabrication of three-dimensional bioactive scaffolds for living organs and transdermal tissues. This transformative technology enables the precise assembly of biomaterials and living cells, creating structures that mimic the complexity of natural tissues. Advances in bioprinting have facilitated the development of personalized scaffolds for tissue regeneration, wound healing, and transdermal drug delivery systems. This abstract explores cutting-edge innovations in bioactive scaffold design, highlighting their potential to replicate functional organ structures and support transdermal therapeutic applications. Current challenges, such as achieving vascularization and mechanical integrity, are discussed alongside emerging solutions and future directions for clinical translation. Bioprinting stands poised to redefine the landscape of regenerative medicine and transdermal therapeutics.

Ischemic stroke is a serious cerebrovascular disease with limited effective treatments. While stem cell therapy shows promise, ensuring cell survival and integration into neural networks remains a challenge. Recent research shows tissue engineering can greatly fix these flaws. Notably, we focus on the structure–activity relationship of biomaterials. How cell behavior can be most beneficially regulated by changes in the physical structure of the cell carrier itself is certainly a new perspective for cost saving and effectiveness increasing compared to the delivery of expensive biotrophic factors. However, there is a lack of research on biomaterials applied to ischemic stroke, especially in combination with stem cells. No biomaterial has even been approved for clinical trials in stroke. We provide a systematic summary of biomaterials-driven stem cell therapy for ischemic stroke in terms of pathomechanisms, applications, and clinical translational challenges; we attempt to build a bridge from laboratory research to clinical translation in stroke treatment.

Diffuse gliomas are brain tumors that include oligodendroglioma, astrocytoma, and glioblastoma (GBM), the most common and deadly primary brain tumor. A major challenge in glioma treatment is resistance to the first-line chemotherapeutic, temozolomide (TMZ). Plasma membrane properties of cells with increased chemotherapeutic resistance are not well understood, despite the fact that the membrane is the first point of contact with the environment and greatly shapes cell behavior. Plasma membrane glycosylation impacts cell function, and we found significant differences in glycosylation of TMZ-resistant cells. We further identified plasma membrane electrophysiological properties predicting glioma cell TMZ resistance. We enriched cells with higher TMZ resistance by sorting glioma cells based on electrophysiological properties, indicating the relevance of membrane properties to chemotherapeutic resistance. These findings could lead to rapid separation methods for patient tumor cells, a better understanding of the molecular profiles of resistant cells, and novel treatment options for gliomas.