Stem Cell Research & Therapy•2025•DOI: 10.1186/s13287-025-04214-8
The authors wish to note the following correction: The images in Fig. 2D of our paper, which were intended to show Annexin V staining for apoptosis of human dental pulp stem cells (hDPSCs) and HGF-transfected hDPSCs (HGF-hDPSCs) under hypoxic conditions or serum-free media, were incorrect. The original results demonstrated that more apoptotic cells were observed in the hDPSCs group compared to the HGF-hDPSCs group. However, we inadvertently used images of Annexin V staining for apoptosis in human bone marrow mesenchymal stem cells (hBMSCs) and HGF-transfected hBMSCs (HGF-hBMSCs). Upon reviewing the original experimental records, we discovered that the incorrect images were included during the manuscript preparation process due to insufficient verification. We have now provided the correct images for hDPSCs and HGF-hDPSCs in Fig. 2D (see attachment). We sincerely apologize for this oversight. This error occurred because our research group has been extensively engaged in studying the biological characteristics of HGF gene-transfected mesenchymal stem cells. Unfortunately, due to carelessness, we mistakenly selected the wrong images. Nevertheless, our research consistently demonstrates that the anti-apoptotic ability of mesenchymal stem cells (including rBMSCs, hBMSCs, and hDPSCs) is enhanced under hypoxic conditions or serum-free media following HGF gene transfection. The methodology and results remain consistent with our previous studies. After thoroughly reviewing all data and experimental records, we confirm that this correction does not affect the validity of the original study’s results or conclusions.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2025205
Ultraviolet-B (UVB) radiation induces significant skin damage by penetrating into the dermal layer, leading to reactive oxygen species (ROS) generation and triggering cellular necrosis and apoptosis. Conventional sunscreens focus primarily on UVB blocking but are limited in their ability to repair dermal damage due to insufficient permeability. In this study, we discover that chebulinic acid (CA), one of the principal monomers in Terminalia chebula Retz., has superior efficacy in promoting recovery from UVB-induced skin damage compared with other major monomers. Mechanistically, CA’s anti-UVB function involves regulating the expression of IL-6 and IFN-β through activation of the MAPK pathway. To overcome the formidable barrier posed by the skin, we identify mulberry exosome-like nanoparticles (MELNs) as an efficient transdermal delivery system and develop CA@MELNs loaded with CA. Furthermore, we demonstrate that the dissociative CA within the CA@MELNs delivery system significantly enhances both transdermal penetration and anti-UVB efficiency in vitro and in vivo. Our findings suggest the substantial potential of CA as an effective ingredient and CA@MELNs as a robust and accessible platform for mitigating UVB damage.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025065
Stem cell fate is profoundly influenced by a complex interplay of biochemical and biophysical cues, with the latter increasingly recognized for its roles in cellular processes, yet the mechanisms are unclear. Since chromatin accessibility is a critical determinant in the processes of osteogenesis and bone repair, investigating the contributions of open chromatin regions (OCRs) to the intracellular signaling pathways triggered by topographical cues, which lead to osteogenic differentiation is highly valuable. This study explores the impact of the nanotopography of biomaterials on the osteogenic differentiation of human bone marrow stem cells (hBMSCs). By utilizing electrospun poly-L-lactide (PLLA) membranes with random fiber arrangements, we mimic the natural extracellular matrix (ECM) topography to study its effects on hBMSCs, contrasting them with flat PLLA controls. Through high-throughput Assay for Transposase-Accessible Chromatin with sequencing (ATAC-seq) and RNA sequencing (RNA-seq), we reveal that the nanotopography of electrospun surfaces promotes osteogenic differentiation by modulating the chromatin accessibility of the YBX1 gene promoter, leading to its upregulation. Lentiviral knockdown experiments further confirm the crucial role of YBX1, revealing a reversal of the osteogenic effects induced by nanotopography. This study emphasizes the importance of YBX1 in the osteogenic response to the surface topography of biomaterials and suggests that nanotopographical cues could be harnessed to direct stem cell fate. These findings are important for developing biomaterials that promote specific stem cell outcomes in regenerative medicine. Our results further contribute to a deeper understanding of the mechanisms underlying stem cell differentiation in response to environmental cues and pave the way for the rational design of biomaterials with enhanced osteogenic potential. By elucidating the role of chromatin accessibility and specific transcription factors such as YBX1, this study highlights the intricate interplay between cell-material interactions and the intracellular signaling pathways that govern stem cell fate.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21500
BACKGROUND: The role of epigenetic regulatory mechanisms, especially N6-methyladenine (m6A) RNA modification, in muscle cell proliferation, differentiation, and disease development is increasingly being studied. However, the multidimensional mechanism of m6A methylation in sarcopenia still needs to be systematically integrated. OBJECTIVE: To explore the key role of m6A methylation in the occurrence and development of sarcopenia, and to review the latest research progress on the involvement of m6A related regulatory factors in the pathological process of sarcopenia. METHODS: Using "m6A methylation, N6 methyladenine, sarcopenia, muscle atrophy, muscle regeneration, muscle, skeletal muscle" as Chinese keywords, and "m6A RNA methylation, sarcopenia, skeletal muscle, muscle mass loss" as English keywords, CNKI and PubMed were searched to screen high-quality literature in recent years, and the mechanism of action and related signaling pathways of m6A methylation in sarcopenia were summarized. RESULTS AND CONCLUSION: m6A methylation participates in the pathological process of sarcopenia through a dynamic and reversible regulatory network (methyltransferases METTL3/METTL14, demethylases FTO/ALKBH5, reader proteins YTHDF1/YTHDF2, etc.). m6A methylation affects the proliferation and differentiation of skeletal muscle cells by regulating satellite cells, ubiquitin-proteasome system, non-coding RNAs, etc. Most studies are based on cell models or animal experiments, with few clinical sample validation and translational application studies. The feasibility of m6A-related factors as diagnostic markers or therapeutic targets for sarcopenia needs further verification.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2026063
Pancreatic cancer is a highly lethal malignancy with a five-year survival of only 13% overall and 8% for pancreatic adenocarcinoma. KRAS mutations, present in over 90% of cases, drive oncogenesis and metabolic reprogramming, including a glycolytic switch. Glutamine and glutamate play interconnected roles in pancreatic cancer metabolism, with glutamine fueling CA19-9 biosynthesis via the hexosamine pathway. Son et al. (2013) identified a non-canonical glutamine metabolism pathway regulated by KRAS, where glutamine-derived aspartate is processed by GOT1 in the cytoplasm, bypassing GLUD1. However, pancreatic tumors are often nutrient-deficient, and under glutamine deprivation, cells may rewire glucose metabolism to generate glutamate. This study analyzed 684 pancreatic adenocarcinoma patients from a prospective database (2021-2025) and found that only 19.6% had normal fasting glucose, with high fasting blood glucose (≥126 mg/dL) being an adverse prognostic factor (HR=1.41, 95% CI 1.07-1.86, P=0.015). Using isotope tracing with D-glucose-13C6 in KRAS-mutated pancreatic cancer cells deprived of glutamine, we observed that glucose-derived carbons were incorporated into glutamate and related metabolites, including glycosylation precursors (UDP-GalNAc), collagen/stroma components (proline, 5-oxoproline), cell division metabolites (adenosine, AMP, ADP, etc.), and ROS-related molecules (GSH, GSSG, γ-glutamylcysteine) at 24h, with additional labeling in UDP-GlcNAc, glycine, and citrate at 48h. These findings suggest that glucose can serve as a potential source of glutamate under glutamine deprivation, providing a metabolic adaptation mechanism for KRAS-mutated pancreatic cancer cells. This rewiring may contribute to tumor progression and represents a potential therapeutic target.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2026035
Pulmonary fibrosis (PF) is a life-threatening interstitial lung disease characterized by scarring and inflammation in lung tissues. Aberrant activation of the JAK/STAT and NF-κB signaling pathways is critical in initiating and sustaining the inflammatory processes that drive fibrotic progression. In this study, we identify a novel small-molecule compound, T4015, a 4-indolyl-2-phenylaminopyrimidine derivative, as a dual-pathway inhibitor targeting both JAK/STAT and NF-κB signaling. Dual-luciferase reporter assays demonstrate the potent inhibitory activity of T4015 against these pathways. T4015 effectively suppresses the phosphorylation of STAT3, JAK1, and TYK2 induced by IL-6 and IFN-β, while suppressing LPS-induced NF-κB activation in macrophages. Transcriptome sequencing and pathway enrichment analyses further confirm that T4015 downregulates multiple inflammation-related signaling cascades, including the JAK/STAT, NF-κB, TNF, IL-17, and Toll-like receptor pathways. In a mouse model of bleomycin-induced PF, T4015 treatment significantly improves survival, attenuates collagen deposition, and reduces the expression of pro-inflammatory and profibrotic markers such as IL-6, CCL2, and COL1. Molecular docking and target prediction analyses suggest that T4015 exhibits strong binding affinity for multiple kinases within the JAK/STAT and NF-κB networks, including JAK1, TYK2, JAK2, JAK3, RIPK1, IRAK1/4, TAB1, and ZAP70. Collectively, these results highlight T4015 as a promising therapeutic candidate for PF through its simultaneous inhibition of the JAK/STAT and NF-κB signaling pathways.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025065
Stem cell fate is profoundly influenced by a complex interplay of biochemical and biophysical cues, with the latter increasingly recognized for its roles in cellular processes, yet the mechanisms are unclear. Since chromatin accessibility is a critical determinant in the processes of osteogenesis and bone repair, investigating the contributions of open chromatin regions (OCRs) to the intracellular signaling pathways triggered by topographical cues, which lead to osteogenic differentiation is highly valuable. This study explores the impact of the nanotopography of biomaterials on the osteogenic differentiation of human bone marrow stem cells (hBMSCs). By utilizing electrospun poly-L-lactide (PLLA) membranes with random fiber arrangements, we mimic the natural extracellular matrix (ECM) topography to study its effects on hBMSCs, contrasting them with flat PLLA controls. Through high-throughput Assay for Transposase-Accessible Chromatin with sequencing (ATAC-seq) and RNA sequencing (RNA-seq), we reveal that the nanotopography of electrospun surfaces promotes osteogenic differentiation by modulating the chromatin accessibility of the YBX1 gene promoter, leading to its upregulation. Lentiviral knockdown experiments further confirm the crucial role of YBX1, revealing a reversal of the osteogenic effects induced by nanotopography. This study emphasizes the importance of YBX1 in the osteogenic response to the surface topography of biomaterials and suggests that nanotopographical cues could be harnessed to direct stem cell fate. These findings are important for developing biomaterials that promote specific stem cell outcomes in regenerative medicine. Our results further contribute to a deeper understanding of the mechanisms underlying stem cell differentiation in response to environmental cues and pave the way for the rational design of biomaterials with enhanced osteogenic potential. By elucidating the role of chromatin accessibility and specific transcription factors such as YBX1, this study highlights the intricate interplay between cell-material interactions and the intracellular signaling pathways that govern stem cell fate.