Stem Cell Research & Therapy•2026•DOI: 10.1186/s13287-026-04964-z
Background Psoriasis is a refractory immune-related disease. In recent years, it has been discovered that mesenchymal stem cells (MSCs) can be used as a new therapeutic approach for psoriasis, but their potential therapeutic mechanism remains unclear. This study aims to explore the role of MSCs in the treatment of psoriasis. Methods We employed a mouse psoriasis model induced by imiquimod (IMQ) in vivo and a co-culture system of MSCs and HaCaT keratinocytes (KCs) cell line in vitro. These approaches allowed us to investigate the effect of MSCs on the levels of inflammatory factors and the activation of inflammasomes in both contexts. Mouse-targeted amino acid sequencing, transmission electron microscopy for in vitro observation, immunofluorescence for both in vivo and in vitro analyses, and siRNA transfection in vitro were employed in this study. Results Our results showed that MSCs significantly improved the skin lesion of mice with psoriasis, and reduced the levels of inflammatory factors and chemokines including IL-1β, IL-6, IL-8, TNF-α, MCP-1, CCL7, CCL20 and CCL27 in the mouse skin lesion areas and M5- induced psoriatic KCs models in vitro. Likewise, MSCs repaired the skin barrier by enhancing claudin-1 expression in vivo. In addition, MSCs increased KRT1 and decreased KRT6 levels in vivo and in vitro. Amino acid metabolism analysis showed that MSCs could improve the serine metabolism level in the mouse skins and upregulated the key enzyme phosphoserine phosphatase (PSPH) in serine metabolism. In vitro experiments demonstrated that knockdown of PSPH could reverse the therapeutic effects of MSCs on psoriasis. Furthermore, studies in vitro and in vivo revealed that MSCs can activate the PINK1-Parkin pathway. It was specifically manifested by elevated levels of PINK1, Parkin, p-Parkin, Beclin-1, and LC3B-II/I, coupled with a reduction in P62 protein. Subsequently, the activation of PINK1-Parkin led to decreased expressions of IL-1β, IL-6, IL-8, TNF-α, CCL7, CCL20, CCL27, and MCP-1. In vitro and in vivo experiments indicated that MSCs can reduce the levels of IL-1β, IL-6, IL-8, TNF-α, CCL7, CCL20, CCL27, and MCP-1 by inhibiting the activation of NLRP3 inflammasomes. Meanwhile, PSPH knockdown in vitro can reverse the activating effects of MSCs on the PINK1-Parkin, as shown by decreased levels of PINK, Parkin, p-Parkin, Beclin-1, and LC3B-II/I, concurrently with an elevation in P62. Conclusions The results of this study indicated that MSCs can alleviate IMQ-induced psoriasiform dermatitis in mice by upregulating serine metabolism. The key serine metabolism enzyme PSPH may enhance PINK1/Parkin-mediated mitochondrial autophagy in psoriatic HaCaT and inhibit NLRP3 inflammasome activation in HaCaT cells, thereby alleviating skin inflammatory responses and suppressing skin proliferation in psoriatic mice.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025031
This is a corrigendum to the article 'Melatonin protects TEGDMA-induced preodontoblast mitochondrial apoptosis via the JNK/MAPK signaling pathway' published in Acta Biochim Biophys Sin (Shanghai) 2024, 56(3): 393–404. In the originally published version, an error was identified in Figure 4A. The corrected figure is provided. This correction does not materially affect the overall findings and conclusions of the paper.
Acta Biochimica et Biophysica Sinica•2024•DOI: 10.3724/abbs.2023263
Resin monomer-induced dental pulp injury presents a pathology related to mitochondrial dysfunction. Melatonin has been regarded as a strong mitochondrial protective bioactive compound from the pineal gland. However, it remains unknown whether melatonin can prevent dental pulp from resin monomer-induced injury. The aim of this study is to investigate the effects of melatonin on apoptosis of mouse preodontoblast cells (mDPC6T) induced by triethylene glycol dimethacrylate (TEGDMA), a major component in dental resin, and to determine whether the JNK/MAPK signaling pathway mediates the protective effect of melatonin. A well-established TEGDMA-induced mDPC6T apoptosis model is adopted to investigate the preventive function of melatonin by detecting cell viability, apoptosis rate, expressions of apoptosis-related proteins, mitochondrial ROS (mtROS) production, mitochondrial membrane potential (MMP) and adenosine triphosphate (ATP) level. Inhibitors of MAPKs are used to explore which pathway is involved in TEGDMA-induced apoptosis. Finally, the role of the JNK/MAPK pathway is verified using JNK agonists and antagonists. Our results show that melatonin attenuates TEGDMA-induced mDPC6T apoptosis by reducing mtROS production and rescuing MMP and ATP levels. Furthermore, mitochondrial dysfunction and apoptosis are alleviated only by the JNK/MAPK inhibitor SP600125 but not by other MAPK inhibitors. Additionally, melatonin downregulates the expression of phosphorylated JNK and counteractes the activating effects of anisomycin on the JNK/MAPK pathway, mimicking the effects of SP600125. Our findings demonstrate that melatonin protects mDPC6T cells against TEGDMA-induced apoptosis partly through JNK/MAPK and the maintenance of mitochondrial function, offering a novel therapeutic strategy for the prevention of resin monomer-induced dental pulp injury.
Stem Cell Research & Therapy•2026•DOI: 10.1186/s13287-026-04964-z
Psoriasis is a chronic inflammatory skin disease affecting 2-3% of the global population. Mesenchymal stem cells (MSCs) have emerged as a potential therapy, but the underlying mechanisms remain unclear. This study investigated the therapeutic effects of adipose-derived MSCs on imiquimod (IMQ)-induced psoriasis in mice and M5-induced psoriatic HaCaT keratinocytes in vitro. MSCs significantly ameliorated skin lesions, reduced inflammatory cytokines (IL-1β, IL-6, IL-8, TNF-α) and chemokines (MCP-1, CCL7, CCL20, CCL27), and restored skin barrier function by upregulating claudin-1. MSCs also normalized keratinocyte differentiation markers (increased KRT1, decreased KRT6). Amino acid metabolomics revealed that MSCs enhanced serine metabolism in mouse skin, upregulating phosphoserine phosphatase (PSPH). Knockdown of PSPH reversed the therapeutic effects of MSCs in vitro. Mechanistically, MSCs activated the PINK1-Parkin mitophagy pathway, as evidenced by increased PINK1, Parkin, p-Parkin, Beclin-1, and LC3B-II/I ratios, and decreased P62. This activation attenuated NLRP3 inflammasome activation and restrained keratinocyte hyperproliferation. The study concludes that MSCs alleviate psoriasis via PSPH-mediated activation of PINK1-Parkin mitophagy, suppressing NLRP3 inflammasome. Limitations include the need to identify specific MSC-secreted factors and lack of clinical validation. These findings provide a rationale for developing PSPH-targeted therapies for psoriasis.
Stem Cell Research & Therapy•2026•DOI: 10.1186/s13287-026-04964-z
Background: Psoriasis is a refractory immune-related disease. In recent years, it has been discovered that mesenchymal stem cells (MSCs) can be used as a new therapeutic approach for psoriasis, but their potential therapeutic mechanism remains unclear. This study aims to explore the role of MSCs in the treatment of psoriasis. Methods: We employed a mouse psoriasis model induced by imiquimod (IMQ) in vivo and a co-culture system of MSCs and HaCaT keratinocytes (KCs) cell line in vitro. These approaches allowed us to investigate the effect of MSCs on the levels of inflammatory factors and the activation of inflammasomes in both contexts. Mouse-targeted amino acid sequencing, transmission electron microscopy for in vitro observation, immunofluorescence for both in vivo and in vitro analyses, and siRNA transfection in vitro were employed in this study. Results: Our results showed that MSCs significantly improved the skin lesion of mice with psoriasis, and reduced the levels of inflammatory factors and chemokines including IL-1β, IL-6, IL-8, TNF-α, MCP-1, CCL7, CCL20 and CCL27 in the mouse skin lesion areas and M5-induced psoriatic KCs models in vitro. Likewise, MSCs repaired the skin barrier by enhancing claudin-1 expression in vivo. In addition, MSCs increased KRT1 and decreased KRT6 levels in vivo and in vitro. Amino acid metabolism analysis showed that MSCs could improve the serine metabolism level in the mouse skins and upregulated the key enzyme phosphoserine phosphatase (PSPH) in serine metabolism. In vitro experiments demonstrated that knockdown of PSPH could reverse the therapeutic effects of MSCs on psoriasis. Furthermore, studies in vitro and in vivo revealed that MSCs can activate the PINK1-Parkin pathway. It was specifically manifested by elevated levels of PINK1, Parkin, p-Parkin, Beclin-1, and LC3B-II/I, coupled with a reduction in P62 protein. Subsequently, the activation of PINK1-Parkin led to decreased expressions of IL-1β, IL-6, IL-8, TNF-α, CCL7, CCL20, CCL27, and MCP-1. In vitro and in vivo experiments indicated that MSCs can reduce the levels of these inflammatory factors by inhibiting the activation of NLRP3 inflammasomes. Meanwhile, PSPH knockdown in vitro can reverse the activating effects of MSCs on the PINK1-Parkin, as shown by decreased levels of PINK, Parkin, p-Parkin, Beclin-1, and LC3B-II/I, concurrently with an elevation in P62. Conclusions: The results of this study indicated that MSCs can alleviate IMQ-induced psoriasiform dermatitis in mice by upregulating serine metabolism. The key serine metabolism enzyme PSPH may enhance PINK1/Parkin-mediated mitochondrial autophagy in psoriatic HaCaT and inhibit NLRP3 inflammasome activation in HaCaT cells, thereby alleviating skin inflammatory responses and suppressing skin proliferation in psoriatic mice.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21305
OBJECTIVE: Upper limb dysfunction after stroke is a common complication that seriously affects the quality of life and daily activity of patients. Virtual reality technology, as an emerging rehabilitation method, can effectively promote neural remodeling and functional recovery. This study will systematically evaluate the therapeutic effects of different virtual reality devices on upper limb motor dysfunction in patients with stroke. METHODS: The China National Knowledge Infrastructure (CNKI), WanFang Database, VIP website, PubMed, Web of Science, Embase, and the Cochrane Library were searched to retrieve relevant literature. Relevant data were extracted, and their quality was assessed. The control group received conventional rehabilitation treatment, while the experimental group received virtual reality rehabilitation training in addition to the treatment provided to the control group. Statistical analysis was performed using RevMan 5.4 and Stata 18.0 software. RESULTS: (1) A total of 12 articles and 571 patients were included in the meta-analysis. (2) Meta-analysis results showed that the Fugl-Meyer score of the upper limb in the virtual reality group was 7.29 times that of the conventional group (MD=7.29, 95%CI: 5.60-8.98, P < 0.05); the Action Research Arm Test score in the virtual reality group was 10.69 times that of the conventional group (MD=10.69, 95%CI: 4.96-16.43, P < 0.05); the modified Barthel index score in the virtual reality group was 8.25 times that of the conventional group (MD=8.25, 95%CI: 3.38-13.12, P < 0.05). (3) Subgroup analysis showed that patients aged 50-59 years had better improvement in upper limb Fugl-Meyer score; patients with disease duration within 3 months had better improvement; intervention duration ≥4 weeks had the best improvement. (4) Network meta-analysis showed that smart glove intervention [MD=-1.05, 95%CI(-1.85, -0.24), P < 0.05] was most effective for improving upper limb motor function; Armeo Spring intervention [MD=-1.19, 95%CI(-1.87, -0.51), P < 0.05] was most effective for improving upper limb coordination; Kinect intervention [MD=-0.59, 95%CI(-1.13, -0.06), P < 0.05] was most effective for improving hand dexterity; VREX intervention [MD=-0.76, 95%CI(-1.28, -0.23), P < 0.05] was most effective for improving activities of daily living. CONCLUSION: For improving upper limb motor function, the smart glove system is the first choice; for improving upper limb coordination, the Armeo Spring system is the first choice; for improving hand dexterity, the Kinect system is the first choice; for improving activities of daily living, the VREX system is the first choice. This study has certain limitations, and the above conclusions should be interpreted with caution.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21562
BACKGROUND: Previous studies have confirmed that the Bushen Jianpi Huoxue Formula can increase bone mineral density in osteoporotic rats. OBJECTIVE: To investigate the effect of Bushen Jianpi Huoxue Formula on bone loss and trabecular biomechanical parameters in ovariectomized rats. METHODS: Fifty female Sprague-Dawley rats were randomly divided into five groups: normal group (n=10) without any intervention, sham-operated group (n=10) with removal of adipose tissue near the ovaries, ovariectomized group (n=10), Bushen Jianpi Huoxue Formula group (n=10), and alendronate group (n=10). The latter three groups underwent bilateral ovariectomy to establish osteoporosis models. After 12 weeks of modeling, the Bushen Jianpi Huoxue Formula group and alendronate group were administered the respective drugs by gavage once daily for 12 weeks, while the other three groups received normal saline. After treatment, lumbar spine bone mineral density was measured, micro-CT analysis of the distal femur and proximal tibia was performed, hematoxylin-eosin staining was used to observe the histological morphology of the proximal tibia, and finite element analysis was used to analyze the strain and stress of the distal femur. RESULTS AND CONCLUSION: (1) The lumbar spine bone mineral density in the ovariectomized group was lower than that in the normal and sham-operated groups (P < 0.05), while the Bushen Jianpi Huoxue Formula and alendronate groups had higher lumbar spine bone mineral density than the ovariectomized group (P < 0.05). (2) Micro-CT analysis showed that compared with the normal and sham-operated groups, the ovariectomized group had lower bone volume fraction, bone surface density, and trabecular number in the proximal tibia (or distal femur) (P < 0.05), and higher trabecular separation and structure model index (P < 0.05). Compared with the ovariectomized group, the Bushen Jianpi Huoxue Formula and alendronate groups had higher bone volume fraction, bone surface density, and trabecular number in the distal femur (P < 0.05), and lower trabecular separation and structure model index in the distal femur (P < 0.05); in the proximal tibia, bone volume fraction, bone surface density, and trabecular number were also higher (P < 0.05). (3) Hematoxylin-eosin staining showed that the degree of bone marrow fat infiltration in the ovariectomized group was higher than that in the normal and sham-operated groups, while the Bushen Jianpi Huoxue Formula and alendronate groups showed significant improvement. (4) Finite element analysis showed that under the same load, the trabecular stress and strain in the ovariectomized group were higher than those in the normal and sham-operated groups (P < 0.05), while the Bushen Jianpi Huoxue Formula and alendronate groups had lower trabecular stress and strain than the ovariectomized group (P < 0.05). These results indicate that Bushen Jianpi Huoxue Formula can prevent bone loss and improve trabecular biomechanical properties in ovariectomized rats, suggesting potential efficacy in preventing osteoporotic fractures.