Biomaterials play a central role in tissue engineering and regeneration by providing scaffolds that support cell adhesion, proliferation and differentiation while modulating the surrounding microenvironment. They represent promising alternatives to traditional surgical approaches that may lead to complications or tissue damage, and their performance is influenced by chemical composition, mechanical behavior, architecture and interfacial properties, all of which can be precisely tuned through advanced fabrication and surface modification strategies. This review synthesizes evidence from a comprehensive literature search across major scientific databases, focusing on highly cited studies and available clinical data, and examines natural and synthetic biomaterials, their biological responses, functional characteristics, and surface modification methods. Emphasis is placed on Cold Atmospheric Plasma (CAP), which selectively modifies the outermost nanolayer of materials, enhancing hydrophilicity, functional group density, protein adsorption and overall cell–material interactions, as well as improving drug loading capacity. The review also considers stem cell interactions with biomaterials and emerging applications of artificial intelligence (AI) for predicting performance and guiding material optimization. Overall, the analysis highlights that natural matrices provide intrinsic bioactivity, synthetic polymers offer tunable mechanics and degradation profiles, and composite systems integrate these advantages. Advances in technologies such as electrospinning and 3D/4D printing enable precise control over architecture, supporting cell colonization and vascularization. Collectively, developments in CAP treatments and AI-driven design strategies are strengthening the regenerative potential of biomaterials and advancing their clinical translation.

GvHD still remains, despite the continuous improvement of transplantation platforms, a fearful complication of transplantation from allogeneic donors. Being able to separate GvHD from GvL represents the greatest challenge in the allogeneic transplant setting. This may be possible through continuous improvement of cell therapy techniques. In this review, current cell therapies are taken into consideration, which are based on the use of TCR alpha/beta depletion, CD45RA depletion, T regulatory cell enrichment, NK-cell-based immunotherapies, and suicide gene therapies in order to prevent GvHD and maximally amplify the GvL effect in the setting of haploidentical transplantation.

Low-dose aspirin is a cornerstone of cardiovascular prevention in high-risk patients, inhibiting platelet cyclooxygenase (COX-1) and reducing thromboxane A2 (TXA2) production for 24 hours. However, the duration of this effect varies among individuals, and the role of inflammation and platelet microRNAs in this variability remains unclear. This study identifies a thromboinflammatory mechanism linked to shorter duration of TXB2 suppression during aspirin therapy. This mechanism involves (1) elevated circulating S100A8/A9, indicating systemic inflammation; (2) reduced platelet microRNA-21-5p (miR-21-5p) and increased circulating miR-21-5p (c–miR-21-5p), suggesting altered microRNA regulation; (3) S100A8/A9-driven upregulation of platelet multidrug resistance protein 4 (MRP4); and (4) enhanced COX-1 expression, resulting in increased TX production. Patients with accelerated COX-1 recovery had increased circulating S100A8/A9 and platelet MRP4, directly related with serum TXB2 and platelet COX-1 mRNA/protein levels. In vitro, recombinant S100A8/A9 (rS100A8/A9) upregulated MRP4 and COX-1 in platelets and DAMI, a human megakaryoblastic cell line, and MRP4 inhibition prevented this effect. Additionally, these patients exhibited lower platelet miR-21-5p levels and higher c–miR-21-5p, inversely and directly related, respectively, to S100A8/A9, MRP4, and serum TXB2 slope. In DAMI cells, rS100A8/A9 reduced platelet miR-21-5p and increased c–miR-21-5p, effects prevented by MRP4 inhibition. During immune inflammation, reflected by high circulating S100A8/A9, once-daily aspirin may incompletely inhibit COX-1 due to miR-21-5p downregulation, higher megakaryocyte/platelet MRP4 expression, COX-1 upregulation driving platelet activation, and c–miR-21-5p release. Circulating S100A8/A9 and miR-21-5p can serve as biomarkers for patients with shorter duration of aspirin effect over 24 hours and potential targets to optimize antiplatelet therapy for high-risk patients.

Oxidative stress (OS), derived from an imbalance between reactive oxygen species (ROS) accumulation and impaired antioxidant defense, is a recognized cause of atherothrombosis, through a complex interaction between low-grade inflammation and platelet activation.

GvHD still remains, despite the continuous improvement of transplantation platforms, a fearful complication of transplantation from allogeneic donors. Being able to separate GvHD from GvL represents the greatest challenge in the allogeneic transplant setting. This may be possible through continuous improvement of cell therapy techniques. In this review, current cell therapies are taken into consideration which are based on the use of TCR alpha/beta depletion, CD45 RA depletion, T regulatory cells enrichment, NK cell-based immunotherapies and suicide gene therapies in order to prevent GvHD and maximally amplify the GvL effect in the setting of haploidentical transplantation.