Objective This study aimed to investigate the protective effect of a metformin (Met)-adipose-derived mesenchymal stem cell exosome (ADSC-Exo) complex (Met-Exo) against hepatic ischemia-reperfusion injury (IRI) and to determine whether this protection is mediated through the silent information regulator 1(SIRT1)-tissue inhibitor of metalloproteinase 3(TIMP3) axis. Methods Met-Exo was constructed and characterized by nanoparticle tracking analysis, Western blotting, and transmission electron microscopy (TEM). An in vitro model of hepatic IRI was established in mouse hepatocyte AML12 cells subjected to oxygen-glucose deprivation/re-oxygenation (OGD/R). Cell viability, apoptosis, and hepatocyte function markers (AST and ALT) were measured to compare the protective effects of Met-Exo, ADSC-Exo, and Met alone. A TranswellTM co-culture system was used to evaluate how macrophage polarization influences OGD/R-induced AML12 injury. AML12 cells were assigned to the following groups: Ctrl, OGD/R, Met, ADSC-Exo, Met-Exo, and macrophage-polarization groups (M0, M1, M1+Met-Exo, M1+pcDNA3.1, M1+pcDNA3.1-SIRT1, M1+pcDNA3.1-TIMP3). SIRT1 and TIMP3 protein levels in AML12 cells were determined by Western blot. Macrophage-polarization markers-inducible nitric-oxide synthase (iNOS) and arginase 1 (Arg1) were also quantified. In parallel, AML12 cells' viability, apoptosis, and hepatocellular function indices (AST& ALT) were assessed. A murine hepatic IRI model was constructed, and Met-Exo was administered to assess therapeutic efficacy in vivo. Results Met-Exo was successfully prepared. In vitro, Met-Exo attenuated OGD/R-induced hepatocyte injury, increased viability, reduced apoptosis, and lowered AST and ALT release. Met-Exo pre-treatment suppressed expression of the M1 marker iNOS and enhanced expression the M2 marker Arg1, thereby alleviating OGD/R damage in AML12 cells. OGD/R markedly decreased SIRT1 and TIMP3 expression in AML12 cells, whereas Met-Exo pre-treatment significantly up-regulated SIRT1 and consequently TIMP3 expression. In macrophage polarization experiments, M1 macrophages exacerbated AML12 injury, shown as decreased protein expression of SIRT1 and TIMP3, increased iNOS levels, reduced Arg1 levels, along with diminished AML12 cell viability, increased apoptosis, and elevated AST/ALT. Over-expression of either SIRT1 or TIMP3 reversed these detrimental effects, skewing macrophages toward the M2 phenotype and mitigating AML12 injury. In vivo, Met-Exo markedly ameliorated hepatic IRI in mice. Conclusion Met-Exo protects against hepatic IRI by activating the SIRT1-TIMP3 axis, thereby driving macrophage polarization toward the anti-inflammatory M2 phenotype, attenuating inflammation and apoptosis in hepatocytes subjected to OGD/R.

To analyze on the role of long-chain non coding ribonucleic acid (LncRNA) plasmacytoma variant translocation 1 (PVT1) in the differentiation of dental pulp mesenchymal stem cells (DPMSCs) into dentin by targeting microribonucleic acid 18b-5p(miR-18b-5p).

To establish an in vitro model of aged murine myogenic cell line C2C12, clarify rhein's anti-inflammatory function, and explore its effects on myogenic induction activity and related immunomodulatory mechanisms in aged C2C12 cells.

To evaluate the effects of cyclic tensile strain on osteogenic differentiation and angiogenic activity of mouse pericytes (PCs).

Objective: To investigate the effect and underlying molecular mechanism of interleukin-10 (IL-10) secreted by M2 macrophages on the osteogenic differentiation ability of rat bone marrow mesenchymal stem cells (BMMSCs) after irradiation. Methods: Between February 2024 and April 2025, eight healthy male SD rats aged 2 to 3 weeks were selected, primary BMMSCs and macrophages from SD rats were cultured in vitro. Macrophages were polarized to the M2 phenotype, and their surface markers were identified by flow cytometry and immunofluorescence. The experiment was divided into four groups: normal BMSC control group (CON), 4 Gy irradiation group (4Gy), 4 Gy irradiation+M2 macrophage co-culture group (4Gy+8 μm), and 4 Gy irradiation+M2 macrophage co-culture+IL-10 neutralizing antibody group(4Gy+8 μm+m/r IL-10). An in vitro cellular irradiation model was established by exposing BMMSCs to X-ray radiation at a dose of 4 Gy. A non-contact co-culture system between M2 macrophages and irradiated BMMSCs was established using Transwell chambers with an 8 μm pore size. After 48 hours of co-culture, ELISA was used to detect the IL-10 concentration in the supernatant of each group, and Western blot was used to measure the expression levels of key osteogenic differentiation markers (ALP, RUNX2, OCN) and STAT3 signaling pathway-related proteins (p-STAT3, STAT3) in BMMSCs. The specific role of IL-10 was verified by adding an IL-10 neutralizing antibody. Results: Cell counting kit-8 assay results showed that on day 7 post-irradiation, the absorbance value of the 4 Gy Irradiation group (0.241±0.093) was significantly lower than that of the control group (1.794±0.083) (t=21.63, P<0.001). Western blot analysis indicated that the expression levels of osteogenic markers ALP and RUNX2 in the irradiation group (0.819±0.074, 0.785±0.074) were significantly lower than those in the control group (1.000±0.067, 1.000±0.056) (t=3.16, P=0.034; t=4.01, P=0.016, respectively). Immunofluorescence analysis revealed that the fluorescence intensities of RUNX2 and ALP in the irradiation group (19.932±1.291, 7.316±0.089) were markedly weaker compared to the control group (31.154±3.352, 30.789±1.455). After co-culture with M2 macrophages, the proportion of viable cells in the co-culture group [(77.800±1.758)%] was significantly higher than that in the Irradiation group [(61.933±2.732)%] (P<0.001). Furthermore, the IL-10 concentration in the supernatant of the co-culture group [(46.39±1.879) pg/mL] was significantly higher than that in the irradiation group [(7.530±0.239) pg/mL] (t=36.74, P<0.001). Western blot results demonstrated that the expression levels of ALP, RUNX2, and OCN in the co-culture group (0.879±0.020, 1.045±0.059, 1.173±0.082, respectively) were significantly higher than those in the Irradiation group (0.749±0.031, 0.858±0.050, 0.785±0.073, respectively) (t=8.07, P=0.015; t=5.01, P=0.038; t=3.07, P=0.918, respectively). Adding 1 μg/ml IL-10 neutralizing antibody to the co-culture system significantly reduced the IL-10 level in the supernatant [(6.521±0.460) pg/mL] compared to the co-culture group [(26.270±6.486) pg/mL] (t=5.06, P=0.037). The p-STAT3/STAT3 ratio in the neutralizing antibody group (0.840±0.071) was significantly lower than that in the co-culture group (1.289±0.156) (t=4.27, P=0.051), and the osteogenic differentiation capacity of BMMSCs was also notably attenuated. Conclusions: M2 macrophages can improve the osteogenic differentiation ability of BMMSCs after irradiation damage by secreting IL-10 and activating the STAT3 signaling pathway.

Objective: To explore the regulatory mechanism of transient receptor potential cation channel subfamily M member 2 (TRPM2) on the osteogenic differentiation capacity of bone marrow-derived mesenchymal stem cells (BMSCs), and to clarify the role of TRPM2-regulated mitophagy in the progression of periodontitis. Methods: Twelve TRPM2 gene knockout (TRPM2-/-) mice and twelve wild-type (WT) mice were used in this study. A periodontitis model was established by silk ligation on the maxillary second molars of mice, with sham operation performed in the control group, and the modeling lasted for 10 days. The mice were divided into four groups (n=6 per group): WT sham operation group, WT periodontitis group, TRPM2-/- sham operation group, and TRPM2-/- periodontitis group. In the periodontitis group, silk ligation was performed on the maxillary second molars of mice, while no silk ligation was conducted in the sham operation group. Micro-CT was employed to collect imaging data for three-dimensional reconstruction. CTvox and CTAn v1.15.4.0 software were used to quantify the distance from the cementoenamel junction to the alveolar bone crest (CEJ-ABC) and bone volume fraction (BV/TV) in maxillary bone tissues of the mice in four groups. Statistical analysis was performed subsequently. Immunohistochemical staining was conducted to detect the expression intensity of Runt-related transcription factor 2 (RUNX2) in periodontal tissues in maxillary bone tissues of the mice in four groups. BMSCs were isolated from the femurs of the two types mice and cultured in vitro, followed by induction for osteogenic differentiation. Alizarin red S (ARS) staining and alkaline phosphatase (ALP) staining were used to evaluate the osteogenic differentiation potential of BMSCs. Western blotting (WB) was performed to determine the expression levels of osteogenic-related markers [RUNX2, bone morphogenetic protein 2 (BMP2), ALP, osteopontin (OPN)]. Meanwhile, transmission electron microscopy (TEM) was used to observe intracellular mitophagy status. WB was applied to detect the expression of autophagy-related proteins [Microtubule-associated proteins 1A/1B light chain 3 (LC3), PTEN-induced putative kinase 1 (PINK1), Parkin RBR E3 ubiquitin protein ligase (Parkin)], and immunofluorescence colocalization labeling was used to assess the fluorescence intensity of LC3, Translocase of the outer mitochondrial membrane 20 (Tomm20), and Lysosomal-associated membrane protein (LAMP). Results: No statistically significant differences were observed in bone volume fraction, trabecular number, and trabecular separation between TRPM2-/- and WT mice (all P>0.05). However, the buccal and palatal CEJ-ABC values in the TRPM2-/- periodontitis group [(265.40±21.72) μm and (273.30±17.56) μm, respectively] were significantly lower than those in the WT periodontitis group [(416.50±20.90) μm and (428.00±17.59) μm, respectively] (both P<0.001). In addition, the relative expression level of RUNX2 in periodontal tissues of the TRPM2-/- periodontitis group [(15.03±0.48) %] was significantly higher than that of the WT periodontitis group [(11.95±0.40) %] (P<0.001). In vitro experiments (ALP and ARS staining) demonstrated that the osteogenic differentiation capacity of BMSCs derived from TRPM2-/- mice was significantly enhanced compared with that from WT mice. WB results showed that the expression levels of osteogenic-related markers (RUNX2, BMP2, ALP, OPN) in BMSCs from TRPM2-/- mice were all upregulated compared with WT mice (all P<0.05, respectively), and so as the protein levels of mitophagy-related indicators (LC3 and BECLIN1)(both P<0.001). Furthermore, TRPM2 deficiency remarkably upregulated the expression of proteins related to the PINK1/Parkin pathway (all P<0.001). Conclusions: TRPM2 regulates the osteogenic differentiation capacity of BMSCs through mitophagy, thereby participating in the progression of periodontitis. Therefore, targeting TRPM2 is expected to serve as a novel and effective strategy for the treatment of periodontitis.

Primary myelofibrosis (PMF) is a myeloproliferative neoplasm (MPN) characterized by malignancy derived from hematopoietic stem cells. Compared with polycythemia vera (PV) and essential thrombocythemia (ET), PMF shows a worse clinical prognosis. Therefore, it is essential to explore biological markers for early identification and intervention to delay the process of the disease. Megakaryocytes (MK) play a central role in the pathogenesis and disease progression of PMF. The thrombophilia, the aggravation of myelofibrosis and the transformation to acute myeloid leukemia (AML) in patients with PMF are closely related to the morphological characteristics of MK.Changes in MK morphology are not only regulated by inflammatory mediators, but also influenced by specific genetic factors. This article will review the mechanism of MK morphological changes in PMF and the latest research progress on the prognosis of PMF with MK morphology, so as to provide reference for early clinical diagnosis and treatment.

Acute myeloid leukemia (AML) is a hematological malignancy caused by abnormal proliferation and blocked maturation of hematopoietic stem cells, leading to the accumulation of a large number of immature or abnormal myeloid cells in the bone marrow and blood. Immune escape is one of the core mechanisms underlying the refractory and relapse of AML. Natural killer (NK) cells play a crucial role in immune surveillance and immune killing. In recent years, NK cell-based immunotherapy has experienced rapid development, especially in allogeneic NK cell therapy, chimeric antigen receptor NK (CAR-NK) cell therapy, intelligent NK cell therapy, and combination strategies with other treatments, providing new therapeutic hope for relapsed and refractory AML patients. Traditional Chinese medicine (TCM) also plays a regulatory role in natural killer (NK) cell function. For instance, acupuncture therapy, Chinese herbal compounds, and herbal extracts can enhance the quantity and activity of NK cells, thereby promoting their potential antitumor effects. This review aims to summarize the latest developments in NK cell therapy for AML and provide scientific references for precise treatment strategies of AML.

To identify radiation-responsive CD168+ stromal stem cells in murine long bone-bone marrow tissues and to investigate the mechanisms of hematopoietic support factors Cxcl12 expression.

To explore the effect of body mass index (BMI) on the efficiency of hematopoietic stem cell (HSC) mobilization.

To explore the changes and clinical significance of lymphocyte subsets in peripheral blood of aplastic anemia (AA) pediatric patients with mixed chimerism of dual donors.

To investigate the therapeutic effect of Sanzi Huangshi Pill (SZHSP) on NHD13 myelodysplastic neoplasms (MDS) transgenic mice and its mechanism of regulating NRAS gene expression.

Acute graft-versus-host disease (aGVHD) is a common complication of allogeneic hematopoietic stem cell transplantation. The efficacy of standard first-line glucocorticoid treatment is limited; more than 40% of patients develop steroid-refractory aGVHD with an extremely poor prognosis. In recent years, mesenchymal stromal cell (MSC) as a second-line treatment for steroid-refractory aGVHD has been widely studied worldwide. In 2025, the first domestic MSC product was conditional approved by the National Medical Products Administration for steroid-refractory aGVHD in patients aged 14 years and above in China. In light of this, this article reviews the clinical research progress of MSC in the treatment of steroid-refractory aGVHD, focusing on mechanisms and efficacy evaluation, aiming to deepen the understanding of the clinical potential and existing challenges of MSC.

Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is an important treatment option for adult patients with relapsed/refractory acute lymphoblastic leukemia (ALL) , and achieving complete remission (CR) is a critical step before allo-HSCT. Recent studies have shown that immunotherapy with the bispecific T-cell engager (BiTE) blinatumomab can eliminate residual chemotherapy-resistant B-ALL cells, significantly improve remission rates in patients with relapsed/refractory B-ALL and those with positive minimal residual disease (MRD) , successfully bridge patients to allo-HSCT, and provide additional options for post-transplant relapse management and maintenance therapy. This article reviews the application strategies of blinatumomab in adult B-ALL.

This study aimed to explore the application of CAR-T cell therapy bridging to allogeneic hematopoietic stem cell transplantation (allo-HSCT) in patients with diffuse large B-cell Richter syndrome, and to review recent advances in the diagnosis, pathogenesis, and treatment of this disease. We retrospectively analyzed the diagnosis and treatment course of one patient diagnosed with Richter syndrome at Binzhou Medical University Hospital and reviewed relevant literature. The patient was a 49-year-old female with a history of chronic lymphocytic leukemia (CLL) for over two years, who presented with a progressively enlarging right neck mass, and was ultimately diagnosed with transformation of CLL into diffuse large B-cell lymphoma (DLBCL) , i.e., Richter syndrome. The patient initially achieved a partial response after three cycles of R-DA-EPOCH combined with zanubrutinib therapy. Following disease progression, the treatment regimen was adjusted to a combination of PD-1 monoclonal antibody, CD20 monoclonal antibody, XPO1 inhibitor, and zanubrutinib for one cycle. This was followed by infusion of autologous anti-CD19 CAR-T cells and subsequent bridging to allo-HSCT. Assessments at 3 and 8 months post-transplantation both demonstrated disease complete remission.

Objective: To explore the efficacy and safety of basiliximab for gastrointestinal (GI) chronic graft-versus-host disease (cGVHD) . Methods: This was a retrospective case series. Patients who developed GI-cGVHD after transplantation at the Peking University Institute of Hematology between January 1, 2018, and December 31, 2023, were included. Outcomes included response rate, time to response, overall survival (OS) , and the incidence of neutropenia, anemia, thrombocytopenia, and infections. Results: A total of 41 patients with GI-cGVHD were included, with a median follow-up of 622 (range, 112-2 418) days. All patients received initial therapy including glucocorticoids, calcineurin inhibitors, and/or other immunosuppressive agents (eg, mycophenolate mofetil, mesenchymal stem cells, and sirolimus) . In the basiliximab group (n=25) , baseline diarrhea was grade 2-4 (grade 2, n=4; grade 3, n=18; grade 4, n=3) . Basiliximab was initiated a median of 6 days after initial therapy, and 12 patients (48.0% ) received >4 doses. In the basiliximab group, 22 patients (88.0% ) achieved complete response (CR) . Among patients who achieved CR, 15 (68.2% ) responded within ≤4 doses. In the non-basiliximab group (n=16) , baseline diarrhea was significantly milder than in the basiliximab group (P<0.001) and was grade 1-2 in all patients (grade 1, n=12; grade 2, n=4) . All patients in this group achieved CR. The response rate did not differ significantly between groups (88.0% vs 100.0% , P=0.150) . The 2-year OS rates were 75.4% and 86.7% (P=0.494) , the 2-year cumulative relapse rates were 16.9% and 14.3% (P=0.913) , and the 2-year non-relapse mortality rates were 14.2% and 6.7% (P=0.526) in the basiliximab and non-basiliximab groups, respectively. No new grade 3-4 hepatic or renal dysfunction or cytokine release syndrome was observed in the basiliximab group. In the basiliximab group, neutropenia, anemia, and thrombocytopenia occurred in 24.0% , 28.0% , and 28.0% of patients, respectively. Any infection, viral infection, bacterial infection, and fungal infection occurred in 52.0% , 36.0% , 32.0% , and 4.0% of patients, respectively. Conclusion: Basiliximab may be used to treat GI-cGVHD, with hematologic and infection-related adverse event rates comparable to those of other systemic immunosuppressants. These findings suggest a potential therapeutic option for GI-cGVHD; however, larger prospective studies are needed to further evaluate its safety.

Chronic myelomonocytic leukemia (CMML) is one of myeloid neoplasms originating from hematopoietic stem/progenitor cells, featuring both myelodysplastic and myeloproliferative characteristics. Significant revisions have been made to the diagnostic and classification criteria for CMML in the 5th edition WHO classification (WHO 2022) and the International Consensus Classification (ICC) . Furthermore, besides the previously proposed CMML-specific prognostic scoring system (CPSS) , newer prognostic models such as CPSS-Mol, BLAST, and BLAST-Mol have recently been introduced, incorporating cytogenetic and molecular data. Treatment decisions for CMML patients should be comprehensively determined based on prognostic stratification, considering the patient's symptoms, disease burden (manifested as cytopenias or proliferative features) , evidence of disease progression, as well as individual patient status and preferences. This article provides an overview of diagnostic considerations, prognostic assessment and therapeutic options.

Myelodysplastic neoplasms (MDS) are a group of highly heterogeneous myeloid tumors originating from hematopoietic stem cells, clinically characterized by single or multiple lineage cytopenia with a risk of acute myeloid leukemia transformation. In recent years, significant progress has been made in basic research and the development of novel targeted therapy for MDS, and the 5th edition of the WHO classification has updated the subtypes of MDS. Therefore, the Chinese Society of Hematology, Chinese Medical Association has revised the "Chinese Guidelines for Diagnosis and Treatment of Myelodysplastic Syndromes (2019) " to standardize the diagnosis, differential diagnosis, prognostic assessment, and treatment selection for MDS, thereby better guiding clinical practice.

To summarize the research in tissue regeneration and engineered scaffold materials for the prevention and treatment of lymphedema.

To review the research progress and application prospects of Kartogenin (KGN) in cartilage repair and tissue engineering.