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.

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.

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.

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.

The loss of collagen is one of the core mechanisms of skin aging. Since collagens are among the most abundant proteins in the human body, their dynamic balance is crucial for maintaining the structure and functions of the skin. This paper systematically introduces the functions and action mechanisms of type I, III, IV, VII, and XVII collagens, which play key roles in the process of skin aging. Type I collagen mainly provides mechanical support to the dermis; type III collagen enhances skin elasticity and assists in barrier repair; type IV collagen maintains the stability of the basement membrane; type VII collagen mediates epidermal-dermal anchoring; and type XVII collagen regulates the homeostasis of epidermal stem cells. Furthermore, this paper deeply discusses the research progress in anti-aging strategies based on the mechanism of collagen loss, including the application of antioxidants to reduce oxidative damage to collagen, the use of new active ingredients to stimulate collagen synthesis, and the promotion of endogenous collagen regeneration by supplementing collagen peptides and other methods. This review aims to integrate the functional network of different types of collagens in skin aging, providing new perspectives and ideas for the development of multi-dimensional and synergistic anti-aging strategies.

Cell-cultured meat is an innovative type of meat product produced by culturing stem cells in vitro based on the mechanisms of animal growth and repair. It has gradually become an important research focus and development direction in the field of alternative protein foods. Due to the severe lack of historical experience and data regarding human consumption, its safety has attracted global attention. Allergens and allergenicity are one of the core issues, while this field is still in its infancy. In this work, we systematically identify the potential allergen sources throughout the cell-cultured meat production chain, which cover seed cells, production materials (culture media, scaffolds, and carriers), and manufacturing processes. We review recent advances in allergen evaluation and cross-allergenicity research, as well as the key challenges in this emerging field. This study explores the potential for developing a high-throughput, scientifically robust evaluation system for the allergenicity of cultured meat by integrating theories and methodologies from multiple disciplines. The aim is to provide forward-looking and scientific support for the production, risk assessment, and safety management of cell-cultured meat products.

Acute graft-versus-host disease (aGVHD) remains a severe complication following allogeneic hematopoietic stem cell transplantation, and traditional corticosteroid therapy often demonstrates limited efficacy. This review highlights the recent advances in cellular and targeted immunotherapies for aGVHD. Mesenchymal stem cells show considerable efficacy in steroid-resistant aGVHD and are already in clinical use. Regulatory T cells (Treg), including CAR-engineered Tregs, effectively induce immune tolerance and reduce GVHD incidence. Targeted agents, such as CTLA-4 fusion proteins and α4β7 integrin antibodies, mitigate severe aGVHD by blocking immune activation or T-cell homing. Additionally, tissue-repair factors (e.g., IL-22, GLP-2 analogs) and immunomodulatory molecules (e.g., α1-antitrypsin) offer novel strategies that combine tissue protection with immunomodulation. Collectively, these innovative therapies are driving aGVHD treatment toward precision, high efficacy, and low toxicity, demonstrating a promising clinical potential.

Radiotherapy is an important treatment modality for tumors and is involved in the treatment course of more than 50% of cancer patients. However, resistance to ionizing radiation results in suboptimal radiotherapy efficacy and contributes to tumor recurrence and metastasis at later stages. With the increasing understanding of tumor pathogenesis, cancer stem cell (CSC), characterized by self-renewal capacity and differentiation potential, have attracted growing attention and play key roles in radiotherapy resistance, tumor progression, metastasis, immune evasion, and other processes. Mechanisms including the tumor microenvironment, DNA damage repair, and epithelial-mesenchymal transition (EMT) are critical drivers of CSC-mediated radiotherapy resistance. Reviewing the key pathways involved and identifying CSC-specific therapeutic targets may provide new insights for developing more efficient and less toxic radiotherapy strategies.

Salivary gland diseases are common disorders in the oral and maxillofacial region, mainly classified into two categories: Tumorous and non-tumorous. Non-tumorous salivary gland diseases include various types such as salivary gland inflammation, Sjögren syndrome, granulomatous diseases, and developmental abnormalities. Some of these diseases are local lesions, while others are closely associated with systemic diseases, often accompanied by impaired salivary secretion function, leading to xerostomia and secondary lesions. Over the past more than 20 years, the Salivary Gland Disease Research Center of Peking University School and Hospital of Stomatology has conducted systematic and in-depth studies focusing on the regulation of salivary secretion function by tight junction proteins, the clinicopathological characteristics, prevention and treatment of novel chronic sialadenitis [including immunoglobulin (Ig) G4-related sialadenitis, 131I-induced sialadenitis, and eosinophilic sialodochitis], stem cells from human exfoliated deciduous teeth-based therapy for Sjögren syndrome, and salivary gland developmental abnormalities. These studies provide important references for the basic research, clinical diagnosis and treatment of related diseases.

Chronic obstructive pulmonary disease (COPD) is a highly heterogeneous disorder characterized by progressive destruction and remodeling of the airways and lung parenchyma. It represents a significant global macroeconomic burden. The lung has a substantial capacity for injury repair to maintain homeostasis. However, this repair process is frequently dysfunctional in COPD. As a group of cells with self-renewal and multi-lineage differentiation potential, pulmonary epithelial stem cells play a key role in COPD lung injury repair process, which is crucial for researchers to figure out the specific mechanism. Although research on lung epithelial stem cells in COPD is still in its early stages, significant milestones have been achieved, particularly through the application of multi-omics technologies. Therefore, this review aims to comprehensively discuss the known types of adult lung epithelial stem cells, their associated microenvironments, and differentiation trajectories, and their roles in injury repair in COPD, as well asrelated therapeutic strategies. Such insights could provide new theoretical foundations and targets for COPD treatment.

Dental stem cells (DSCs) are a type of adult stem cells derived from teeth and their surrounding tissues. DSCs have attracted significant attention in tooth and bone regeneration research due to their strong osteogenic/odontogenic differentiation potential. Recent studies have shown that lipid metabolism plays a crucial role in stem cell biological activities and may even serve as a key determinant of cell fate. However, the specific roles and regulatory mechanisms of lipid metabolism in the osteogenic/odontogenic differentiation of DSCs have not yet been systematically summarized or comprehensively elucidated. Based on the latest research advances, we systematically analyzed the changes in lipid metabolism during the osteogenic/odontogenic differentiation of DSCs and explored the key regulatory functions involved in this process, aiming to provide new perspectives on metabolic regulation and potential intervention strategies for regenerative medicine research.

Trained immunity is a state of enhanced immune responsiveness based on innate immune (epigenetic) memory. It has recently been reported that trained immunity plays an important role in the comorbidity of periodontitis and rheumatoid arthritis (RA). Epigenetic modifications in hematopoietic stem and progenitor cells (HSPCs) can activate trained immunity in bone marrow-derived cells, a mechanism closely associated with the onset and progression of periodontitis and other related systemic diseases. Exhibiting hyper-reactivity, trained immune cells are capable of migrating to distant joint sites and eliciting a more intense inflammatory response upon external stimulation. This review focuses on the underlying mechanisms of trained immunity and its involvement in both periodontitis and RA. Understanding the role of trained immunity in the association between periodontitis and RA provides valuable insights for further research and the development of therapeutic strategies for inflammatory comorbidities, such as periodontitis and RA.

Idiopathic Pulmonary Fibrosis (IPF) is a chronic, progressive, and fatal interstitial lung disease. Its pathological hallmark is abnormal scarring (fibrosis) of lung tissue, leading to irreversible loss of pulmonary function. Recent research proposes that IPF fundamentally represents a dysregulated wound healing response. This process initiates with injury to the respiratory epithelium, evolves through imperfect tissue repair, and culminates in pathological remodeling of lung tissue. Dysfunction of lung epithelial tissue stem cells plays a central role in this cascade. In IPF patients, adult lung tissue stem cells, including TP63+ KRT5+ airway basal cell (BC), AXIN2+ alveolar epithelial progenitor (AEP), and SCGB3A2+ respiratory airway secretory cell (RAS), exhibit significant impairment in stemness function. This manifests as increased senescence and aberrant differentiation, resulting in a imperfect wound healing response characterized by insufficient regenerative repair of the respiratory epithelium and active fibrotic repair. Intrapulmonary transplantation of tissue stem cells for IPF patients can achieve functional reconstitution of stem cells within the remodeled epithelium, leading to improvement in fibrotic lesions and lung function. Therapeutic strategies aimed at restoring the balance of lung tissue regeneration via stem cells hold promise for achieving disease control or even reversal in IPF.

In recent years, the incidence of B-cell non-Hodgkin lymphoma (B-NHL) in China has shown a steady increase, accounting for approximately 85%-90% of all lymphomas. Although standard immunochemotherapy regimens such as R-CHOP have led to long-term remission in some patients, approximately 30%-40% still experience relapse or refractory disease, with dismal prognosis and a median survival of less than one year. For patients who fail multiple lines of therapy, conventional options such as chemotherapy, radiotherapy, or hematopoietic stem cell transplantation offer limited benefits, highlighting an urgent need for innovative treatments. Chimeric antigen receptor T-cell (CAR-T) therapy, a breakthrough form of adoptive cellular immunotherapy, modifies autologous T cells to specifically recognize and eliminate malignant B cells, thereby achieving significant survival improvement in patients with relapse or refractory B-NHL. The clinical research and clinical application of CAR-T in the treatment of hematological tumors in China are in a state of rapid development. At present, there are two targeting CD19 CAR-T cells for the treatment of B-cell lymphoma, which gradually changed the diagnosis and treatment practice of lymphoma in China. At the same time, the clinic is actively exploring and improving the whole-process management experience of CAR-T therapy in lymphoma patients. So the Lymphoma Quality Control Expert Committee of the National Cancer Quality Control Center organized experts to form the consensus through discussion and revision many times, aiming to provide better guidance for clinicians to standardize the whole-process management of CAR-T cell therapy for B-cell Lymphoma, and further improve the survival benefits of patients.

Immunotherapy, in particular, chimeric antigen receptor T cells (CAR-T), is known as a critical approach for the treatment of patients with hematological malignancies. However, there are still huge challenges in the treatment of solid tumors. Therefore, further studies are required to the application of CAR technology to other types of immune cells, for example, CAR-macrophages (Mϕ). Human pluripotent stem cells (hPSC) can be genetically modified either by viral and non-viral methods at clonal level and efficiently differentiate into Mϕ. Therefore, hPSC provide an important platform to produce large scale of genetically engineered Mϕ. CAR engineering Mϕ can enhance the targeted recognition ability, antigen presentation function, cytokine secretion and immune cell recruitment, thereby improving its anti-tumor activity. In the current review, we summarize the current methods for differentiating hPSC into Mϕ, the engineering strategies of CAR-Mϕ, and the current antitumor applications to treat solid tumors. Meanwhile, we focus on the application prospects and challenges of hPSC-derived CAR-Mϕ in solid tumors. Furthermore, we comprehensively analyze the potential of CAR-Mϕ in the field of cell therapy, and deeply explore the unique advantages of Mϕ. This review might provide the potential ideas and new directions for future research and application.

Stroke is the leading cause of death and disability in China and the second in the world. A large number of neurons died after ischemic stroke. Due to the limited regenerative capacity of central nervous system, severely restricted neuronal regeneration leads to permanent functional impairment. Therefore, the key to the restoration of ischemic stroke is the regeneration of functional neurons through various strategies. Endogenous neural stem cells are present in the adult central nervous system throughout life and are capable of continuously generating new neurons. This is the intrinsic basis for using endogenous neural stem cells to repair ischemic stroke. Focusing on neuronal regeneration, this review summarizes the changes of endogenous neurogenesis after ischemic stroke. In particular, this review discusses new strategies for the treatment of ischemic stroke by enhancing endogenous repair mechanisms, which provides a theoretical basis for targeting endogenous neurogenesis for the treatment of ischemic stroke.