Primary malignant cardiac tumours are very rare, with a reported incidence ranging from 0.0017% to 0.07%. Intimal sarcomas originate from subendothelial multifunctional stem cells and occur predominantly in older individuals, affecting large arteries. Cardiac localization is extremely rare.

Acute graft-versus-host disease (aGvHD) is a potentially life-threatening complication that can occur following allogeneic haematopoietic stem cell transplantation. Although corticosteroids remain the standard first-line therapy, a considerable number of patients fail to respond adequately, leading to significant morbidity.

Nanozymes are a class of nanomaterial-based catalysts with enzyme-like functionalities. They exhibit excellent physicochemical properties and stable catalytic activity in both in vivo and in vitro environments, demonstrating immense potential for biomedical applications. Autoimmune diseases arise from the immune system's erroneous attack on self-tissues or cells, affecting individuals across all age groups. Current therapies primarily rely on immunosuppressive drugs, which may control disease progression or alleviate symptoms but often fail to achieve a cure. Long-term use of these drugs is associated with significant side effects, imposing substantial health burdens on patients. Oxidative stress, driven by excessive reactive oxygen species (ROS) production or dysfunctional antioxidant defense systems, is a key mechanism underlying many autoimmune diseases. Excessive ROS accumulation exacerbates cellular damage and inflammatory responses, accelerating disease progression. Nanozymes, with their enzyme-mimicking catalytic capabilities, are ideal tools for modulating ROS levels, offering promising applications in the prevention and treatment of autoimmune diseases. Furthermore, by regulating the ROS microenvironment, nanozymes may enhance the proliferation, differentiation, and regenerative capacity of stem cells, further amplifying their therapeutic potential. This review comprehensively explores recent advancements in nanozymes for biomedical applications, focusing on their roles in oxidative stress modulation and mesenchymal stem cell (MSC)-based therapies. It aims to provide innovative insights and solutions for future clinical strategies.

Inhalation-induced lung injury, caused by harmful factors like chemical fumes and dust, leads to acute and chronic inflammation and fibrosis. Traditional treatments, such as mechanical ventilation and anti-inflammatory drugs, can relieve symptoms but fail to promote tissue regeneration. Stem cells and their extracellular vesicles (EVs) offer new treatment possibilities due to their anti-inflammatory and regenerative properties. However, the specific pathological environment of these lung injuries limits the effectiveness and targeting of EVs, challenging their clinical use. This review outlines stem cell EVs' mechanisms in treating inhalation-induced lung injury, examines recent engineering advancements, and addresses challenges in moving from research to clinical application. It highlights the importance of interdisciplinary collaboration in carrier design, production, and regulation, offering a theoretical foundation for developing precision EV-based treatments.

Polycystic ovary syndrome (PCOS) is a major health concern for women of reproductive age and a leading cause of infertility and metabolic dysfunction. Current treatments mainly involve lifestyle modification and pharmacological therapies, such as oral contraceptives and metformin, and may also include laparoscopic ovarian drilling (LOD), acupuncture, and probiotic interventions. Although these approaches can be effective, they often produce adverse effects and show a high relapse rate after discontinuation. This review summarizes recent advances in exosome-based therapies as emerging strategies for PCOS. Exosomes derived from adipose-derived mesenchymal stem cells, menstrual blood-derived stem cells, bone marrow mesenchymal stem cells, brown adipocytes, and human umbilical cord-derived mesenchymal stem cells have demonstrated therapeutic potential. As nanosized extracellular vesicles carrying bioactive molecules, exosomes exhibit strong targeting capacity and low immunogenicity. We discuss the mechanisms by which exosomes may ameliorate PCOS, including suppression of chronic low-grade inflammation, enhancement of mitochondrial function, inhibition of apoptosis, modulation of angiogenesis, and improvement of metabolic disturbances. However, translating these promising findings into clinical practice faces significant challenges. The main obstacles include lack of standardization, high production costs, and limited clinical data to confirm safety and efficacy. Addressing these issues could pave the way for mechanism-based, personalized exosome treatments and offer new approaches for managing PCOS.

Plant-derived exosome-like nanoparticles (PDENs) have demonstrated unique advantages in the prevention and treatment of osteoporosis and osteoarthritis in recent years. This review systematically summarizes the biological properties of PDENs, methods for their isolation and purification, molecular composition, and their mechanisms of action in bone and joint tissue repair. Current evidence indicates that PDENs can maintain bone homeostasis by promoting the proliferation and differentiation of osteoblasts, inhibiting osteoclast activity, modulating osteogenic differentiation of mesenchymal stem cells, and stimulating angiogenesis. In the context of osteoarthritis, PDENs enhance joint repair by facilitating chondrocyte regeneration, modulating inflammatory responses, and improving extracellular matrix metabolism. Despite the promising therapeutic potential of PDENs in the treatment of bone- and joint-related diseases, challenges remain regarding their precise mechanisms of action, standardization of preparation, and clinical translation. Future research should focus on elucidating the underlying mechanisms, establishing robust quality control methodologies, and conducting comprehensive preclinical evaluations to pave the way for their clinical application.

To analyze the characteristics and research hotspots of perianal lesions associated with Crohn's disease (CD) based on the currently published literature.

Stress fiber-generated traction forces critically regulate mesenchymal stem cell (MSC) behavior, yet how mechanical cues are integrated across transcriptional programs remains unclear. Here, we attenuated actomyosin contractility in human MSCs and performed parallel Assay for Transposase-Accessible Chromatin with high-throughput sequencing (ATAC-seq), YAP-targeted Cleavage Under Targets and Tagmentation sequencing (CUT&Tag) and RNA-seq profiling. We show that reduced stress fiber traction force selectively reorganizes chromatin accessibility into coherent functional modules, resulting in diverse transcriptional programs. The mechanosensitive co-activator YAP functions as a parallel force-responsive regulatory layer coordinating with chromatin accessibility changes. Integration of chromatin accessibility, YAP occupancy, and transcriptomic profiles reveals pathway-specific regulatory responses, identifying focal adhesion and PI3K-Akt signaling as central mechanosensitive pathways coordinated across layers. Together, these findings establish a modular framework for force-dependent gene regulation, demonstrating how mechanical signals are integrated across epigenomic and transcriptional networks to shape MSC transcriptional programs.

This study aimed to critically review the current evidence on the anticancer potential of the cell-derived secretome, with emphasis on mesenchymal stem/stromal cell (MSC) products, and to provide a realistic translational roadmap.

Radiotherapy is an important treatment for lung cancer. However, in the course of radiotherapy, treatment-related side effects and decreased radiosensitivity remain challenging issues. TGF-βR1 can induce radiation-induced bystander effect (RIBE) through the primary cilia; however, this mechanism needs to be further elucidated. At present, traditional Chinese medicine (TCM) shows great advantages in protecting against RIBE, in which Astragalus and its related formulations show good protective effects against radiation; however, the mechanisms by which Astragalus exerts these protective effects are unknown. Therefore, this study aims to investigate the molecular mechanisms by which TGF-βR1 exerts RIBE through the primary cilia, enhancing radiosensitivity, and to reveal the therapeutic effects of small molecules derived from Astragalus membranaceus via this pathway.

Human dental pulp stem cells (hDPSCs) are oral-derived mesenchymal stem cells with high proliferative capacity and odontogenic differentiation potential, making them relevant for dental pulp and dentin–pulp complex regeneration. This in vitro study evaluated the effects of collagen membrane and mineral trioxide aggregate (MTA) conditioned media, individually and in combination, on hDPSC viability, odontogenic differentiation, and mineralization.

Emerging evidence indicates that granzyme K expressing tumor infiltrating CD8 + T-cells play a critical role in mediating anti-tumor T-cell immunity and immunotherapy treatment response. However, precise characterization and cell surface markers for the viable isolation of these cells from tumor samples are lacking.

During weaning, the transition to solid food diversifies the gut microbiome, triggering a programmed immune response critical for long-lasting mucosal immunity. Previous work showed that the gut microbiome mediates epigenetic development in intestinal stem cells (ISCs) during suckling, but what happens during weaning is unclear. Here, genome-wide profiling revealed that weaning-driven microbiome changes shape the DNA methylome and transcriptome of murine ISCs in an IFNγ-dependent manner. Specifically, we observe demethylation of enhancer elements essential for MHC class II genes, which results in a transcriptional memory that persists through differentiation into adulthood. IFNγ blockade, or low-dose penicillin to target Gram-positive bacteria, in early life impaired microbiome-mediated epigenetic control and mucosal immunity, and exacerbated colitis. Murine organoids primed with IFNγ showed rapid, amplified transcriptional responses upon secondary stimulations. These findings reveal that early-life events alter the gut microbiome and these changes reprogramme ISC epigenetic memory to shape mucosal immunity.

Neural cells in the adult human central nervous system (CNS) display extensive transcriptional heterogeneity. How different layers of epigenetic regulation underpin this heterogeneity is poorly understood. Here we profile, at the single-nuclei epigenomic level, distinct regions of the adult human CNS, for chromatin accessibility and simultaneously for the histone modifications H3K27me3 and H3K27ac. We unveil a putative SOX10 enhancer and primed chromatin signatures at HOX loci in spinal-cord-derived human oligodendroglia (OLG) and astrocytes, but not microglia. These signatures in adult OLG were reminiscent of developmental profiles but were decoupled from robust gene expression. Moreover, using high-resolution Micro-C, we show that induced pluripotent stem-cell-derived human OLGs exhibit a HOX chromatin architecture compatible with the primed chromatin in adult OLGs, bearing a strong resemblance not only to OLG developmental architecture but also to high-grade pontine gliomas. Thus, epigenetic memory from developmental states in adult OLG not only enables them to promptly transcribe Hox family genes during regeneration but also makes them susceptible to gliomagenesis.

Ulcerative colitis (UC) is a debilitating, immune-mediated inflammatory disorder of the gastrointestinal (GI) tract with far-reaching consequences on distal organs, including the bone marrow. Here, we describe the molecular mechanisms that contribute to UC-induced abnormal hematopoiesis. We show that chronic UC drives HSPC differentiation toward myelopoiesis in an APE1/Ref-1/HIF-1α/IL-1r1-dependent manner. Blockade of the redox-activity of APE1/Ref-1 with APX3330 inhibits the elevated expression of HIF-1α in HSPCs and reverses the aberrant HSPC dynamics under the inflammatory milieu of UC, including suppression of pro-inflammatory Ly6Chi monocytes. Using echinomycin, we pharmacologically blocked HIF-1α activity and found that HIF-1α mediates inflammatory responses via downstream IL-1r1 signaling. Blockade of the redox activity of ref-1 rescues the abnormal HSPC function. Our data highlight the significance of the APE1/Ref-1/HIF-1α/IL-1r1 signaling cascade in aberrant hematopoiesis that contributes to the pathophysiology of chronic UC through a feed-forward loop.

Glioblastoma (GBM) is often complicated by venous thromboembolism (VTE), primarily driven by tissue factor (TF, F3) and podoplanin (PDPN). These factors promote local hypercoagulation and microthrombosis, thereby contributing to tumor progression by enhancing migration, invasion, and inflammation. Both TF and PDPN can be released via extracellular vesicles (EVs), which carry procoagulant and immunomodulatory cargo. We developed a translational workflow combining biobanked tumor samples, clinical data, ex vivo GBM cultures, and coagulation assays to investigate mechanisms of hypercoagulation. Intraoperative blood coagulation was profiled using ClotPro®. Gene expression of coagulation-related markers was analyzed in tumor tissues and cell lines, complemented by RNAseq-based profiling of coagulation–inflammation links. Functional coagulation assays included clotting time, platelet aggregation, and EV-based analysis of prothrombotic and immunomodulatory activity. Peripheral coagulation in GBM patients was largely unaltered. However, tumor tissues consistently showed high F3 and PDPN expression and markedly low tissue factor pathway inhibitor (TFPI) levels (p < 0.001), indicating a shift toward a procoagulant phenotype. Patient-derived GBM cell lines showed variable TF and PDPN expression, which correlated with clotting potential. Distinct procoagulant mechanisms were observed, with some cells engaging both TF-mediated thrombin generation and PDPN-driven platelet activation. EVs isolated from GBM patient plasma and culture media showed similar procoagulant characteristics, with activity proportional to TF expression, and immune-modulating effects. Notably, GBM-derived EVs modulated microglial behavior, induced senescence, and triggered immune polarization in a cell line-dependent manner, likely contributing to tumor microenvironment remodeling. GBM-associated hypercoagulability is shaped by heterogeneous tumor-intrinsic pathways and EV-mediated mechanisms. The dual role of EVs in promoting coagulation and modulating immune responses provides a mechanistic framework for further studies investigating EVs as potential biomarkers and therapeutic targets relevant to future thromboprophylactic strategies in GBM patients.