MedComm – Biomaterials and Applications最新文献

The intratumoral microbiome has emerged as a critical component of the tumor microenvironment (TME), playing a significant role in tumorigenesis, pathological classification, metastasis, and prognosis. The nutrient-rich, hypoxic, acidic, and immunosuppressive nature of the TME facilitates the establishment of diverse intratumoral microbiome communities. In turn, the intratumoral microbiome further contributes to the formation of cold TME through mechanisms such as genetic and epigenetic alterations, pro-inflammatory responses, immune modulation, tumor metastasis, and enhanced drug resistance. Targeting and eliminating the intratumoral microbiome using nanotechnology presents a unique therapeutic strategy for overcoming chemotherapy resistance and improving the immunosuppressive TME. This review summarizes the microbial characteristics of various tumors and microbiome-mediated oncogenic mechanisms, with particular emphasis on recent advancements in nanotechnology aimed at eliminating the intratumoral microbiome and reprogramming the cold TME, thereby enhancing the efficacy of tumor immunotherapy. Our aim is to provide valuable insights to strengthen the effectiveness of tumor immunotherapy.

Vascular calcification is highly associated with cardiovascular morbidity and mortality among patients with chronic kidney disease (CKD). Despite its clinical severity, no effective therapies exist to halt its progression. Sirtuin 6 (SIRT6) has recently emerged as a promising therapeutic target for vascular calcification. Our prior work demonstrated that SIRT6 activation inhibits vascular calcification by attenuating the osteogenic trans differentiation of vascular smooth muscle cells (VSMCs). While the natural compound cyanidin can activate SIRT6, its clinical translation is hampered by poor bioavailability and the absence of targeted delivery systems. To address this, we developed a dual targeting nanoplatform (TROC) based on Ti₃C₂ nanosheets co-assembled with osteocalcin (OCN) and RANKL antibodies for the targeted delivery of cyanidin. Leveraging data from the Framingham Heart Study offspring cohort and in vitro VSMC models, we first established dietary anthocyanins as an independent protective factor against aortic calcification. We then demonstrated that TROC exhibits excellent stability and dose-dependently reduces calcium deposition in VSMCs. Furthermore, in vivo fluorescence and computed tomography (CT) multimodal imaging confirmed the selective accumulation of TROC at calcification sites and its efficacy in alleviating vascular calcification. This novel drug delivery system represents a promising strategy for advancing the clinical treatment of Vascular calcification.

Lina Papadimitriou, Maria Graigkioti, Eirini, Konstantinos Pagonidis, Yannis Papaharilaou, Anthi Ranella, and Alexandros Lappas. MedComm – Biomaterials and Applications 2025; 4:e70030; pages 1–13.

In the FIRST page, an AUTHOR's name needs attention. Namely:

The text: “Eirini Koutsouroubi¹” is incorrect. This should have read as: “Eirini D. Koutsouroubi¹”.

In the FIRST page, under the AFFILIATIONS, the following need correction. Namely:

First affiliation, the text: “¹Foundation for Research and Technology-Hellas, Institute of Electronic Structure and Laser, Foundation for Research and Technology-Hellas, Heraklion, Crete, Greece” is incorrect. This should have read as: “Institute of Electronic Structure and Laser, Foundation for Research and Technology-Hellas, Heraklion, Crete, Greece”.

Third affiliation, the text: “³Knossos Diagnosis Medical Centre, Department of Medical Imaging, Knossos Diagnosis Medical Centre, Heraklion, Crete, Greece” is incorrect. This should have read as: “Department of Medical Imaging, Knossos Diagnosis Medical Centre, Heraklion, Crete, Greece”.

Fourth affiliation, the text: “⁴Foundation for Research and Technology-Hellas, Institute of Applied and Computational Mathematics, Foundation for Research and Technology-Hellas, Heraklion, Crete, Greece” is incorrect. This should have read as: “Institute of Applied and Computational Mathematics, Foundation for Research and Technology-Hellas, Heraklion, Crete, Greece”.

In the FIRST page, in the ABSTRACT section, the following need correction. Namely:

Lines 4 and 5 from the top, the text “Dynamic light scattering and transmission electron microscopy TEM confirmed” is incorrect. This should have read as “Dynamic light scattering (DLS) and transmission electron microscopy (TEM) confirmed”

We apologize for these errors.

Messenger RNA-loaded lipid nanoparticles (mRNA@LNPs) have achieved remarkable success in vaccine development, but their long-term preservation imposes stringent requirements for transportation and storage. To broaden application of this technology, it is essential to develop LNP formulations with enhanced stability. However, the fundamental rules behind LNP stability remains poorly understood. As a key lipid, the impact of the thermostability of ionizable lipids on LNP formulation's stability remains unexplored. In this study, we investigated the thermostability of two ionizable lipids—an in-house-developed lipid (A1-D1-5) and SM-102, the latter used in FDA-approved mRNA therapeutics—and assessed the stability of LNPs composed of these lipids under various storage conditions. Notably, we found that the size and polydispersity index (PDI) measured by dynamic light scattering (DLS) did not accurately reflect the stability of LNPs. While these indicators showed little change after 44 days of storage at 4°C, the mRNA activity sharply declined within just 14 days of preparation. Additionally, A1-D1-5 demonstrated greater thermostability compared to SM-102, leading to a slower decrease in mRNA activity. Importantly, our findings suggest that replacing ester bonds with amide bonds can significantly improve the thermostability of ionizable lipids. Overall, these results provide valuable insights into optimizing and evaluating the stability of mRNA@LNP formulations.

Lysosome-targeting chimeras (LYTACs) represent a novel class of targeted protein degradation (TPD) technologies that utilize lysosome-targeting receptors (LTRs) to degrade extracellular and membrane-bound proteins. Unlike traditional proteasomal degradation pathways, LYTACs direct target proteins to lysosomes for degradation through receptor-mediated endocytosis, offering a promising solution for targeting previously “undruggable” extracellular proteins. To provide an in-depth analysis of the current state of development, existing challenges, and promising future directions of LYTAC technologies, this review first introduces TPD strategies with a focus on LYTAC. It subsequently enumerates 15 LTRs employed in LYTAC systems, with detailed analysis of 9 representative LTRs and their corresponding targeted protein degradation chimera designs. Additionally, two transmembrane E3 ubiquitin ligases functioning as non-classical LTRs are discussed. Finally, the review concludes by summarizing three major challenges currently facing LYTAC technologies, while presenting potential solutions supported by recent research advancements. This comprehensive analysis aims to provide emerging researchers in the LYTAC field with an updated overview of current developments, while offering valuable insights and research perspectives for scientists actively engaged in LYTAC-related investigations.

Pancreatic cancer, particularly pancreatic ductal adenocarcinoma (PDAC), is very lethal with a poor prognosis. The outcome of traditional treatments for PDAC, including surgery, chemotherapy, and radiotherapy, remains unsatisfactory. Recently, immunotherapy, such as mRNA vaccines, immune checkpoint inhibitors, and chimeric antigen receptor T-cells (CAR-T), has shown encouraging advancement at the early stage and provided new opportunities for pancreatic cancer treatment. However, none of the immunotherapies have induced a significant improvement in the clinical prognosis of PDAC till now. Novel pancreatic cancer therapeutic research and development have attracted scientists' keen interest. Photothermal therapy (PTT) is demonstrated to be able to not only directly induce tumor cell death through localized thermal ablation, but also promote antitumor immune response under appropriate conditions, with the release of damage-associated molecular patterns (DAMPs) and tumor-associated antigens (TAAs) from tumor cells, followed by activation of antigen-presenting cells (APCs) and T cell infiltration to kill tumor cells. This review outlines the current treatment strategies and advances of pancreatic cancer, with a focus on the latest evolving research progress based on PTT and immunotherapy. The application prospects and challenges for photothermal immunotherapy in pancreatic cancer treatment are discussed.

Gan, R., Ni, E., Li, G. and Chen, W. (2025), A New Paradigm for Precision Drug Delivery in Inflammatory Bowel Disease: Effective Transfer, Enhanced Retention, and Pathology-Targeting Treatment via Biomaterials and Engineered Platforms. MedComm – Biomaterials and Applications, 4: e70022.

In the Conflict of Interest, the text “The authors declare no conflicts of interest.” was incorrect. This should have read: “Wei Chen is the editorial board member of MedComm - Biomaterials and Applications, but was not involved in the journal's review of or decisions related to this Manuscript. The other authors declared no conflict of interest.”

The editorial office of MedComm – Biomaterials and Applications apologizes for this error.

Tuberculosis (TB) infects one-quarter of the global population and remains a global health crisis, with persistent diagnostic gaps in sensitivity, speed, and accessibility. Nanobiosensors leverage the unique optical, electrical, and magnetic properties of nanomaterials to enhance signal capture and transduction. Meanwhile, functionalized nanointerfaces reduce interference, enabling portable, multiplexed point-of-care testing (POCT). However, existing platforms are predominantly pathogen-specific, leading to fragmented disease management amidst rising co-infections and antimicrobial resistance. This review introduces a paradigm shift toward modular nanosensing platforms designed for cross-pathogen diagnostic universality. We discuss the engineering principles that unify reconfigurable core nanomaterial scaffolds, plug-and-play biorecognition elements, hierarchical signal amplifiers, and universal sample processors. The plug-and-play approach transforms fragmented, pathogen-specific assays into a cohesive diagnostic platform, facilitating equitable deployment in resource-constrained settings. These platforms dynamically adapt to diverse pathogens, from Mycobacterium tuberculosis (Mtb) to viruses, fungi, and parasites, enabling ultrasensitive detection in complex matrices. By integrating recognition, transduction, and processing, reconfigurable systems offer rapid, low-cost, field-deployable diagnostics. Modular nanosensors utilize functionalized interfaces to amplify trace biomarker capture, reduce interference, and enable multiplexing, advancing high-sensitivity, low-cost infectious disease diagnostics. It charts a roadmap toward equitable global health against antimicrobial resistance, addressing fragmentation to tackle co-infections and emerging pandemics in resource-limited settings.

This study explores the development and characterization of iron oxide nanoclusters (NCs) functionalized with vascular cell adhesion molecule 1 (VCAM-1) for targeted magnetic resonance imaging (MRI) of early atherosclerotic lesions. The NCs were synthesized via a high-temperature polyol method and functionalized using 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide/N-hydroxysuccinimide (EDC/NHS) chemistry to enable conjugation with VCAM-1 antibodies. Dynamic light scattering and transmission electron microscopy TEM confirmed controlled growth of NCs with a size ranging from 40 nm, in the parent to 110 nm post-functionalization, maintaining though colloidal stability in aqueous media. Cytotoxicity assays using mesenchymal stem cells (MSCs) demonstrated high biocompatibility. Confocal and electron microscopy confirmed specific binding of VCAM-1-NCs to VCAM-1-overexpressing MSCs under inflammatory conditions, with internalization through the endolysosomal pathway. The functionalized NCs remained bound under shear stress in an orbital flow model, mimicking early atherosclerotic conditions. MRI phantom analysis demonstrated preserved contrast capability despite increased T₂* relaxation times following antibody conjugation. These findings highlight the potential of VCAM-1-NCs as noninvasive imaging agents for early-stage atherosclerosis and vascular inflammation. Although this study is limited by the lack of in vivo validation and therapeutic evaluation, it provides a strong foundation for future translational research.