Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025105
This review delves into the crosstalk network between oligodendrocytes and other glial cells in the context of demyelinating diseases. Oligodendrocytes, the myelin-forming cells in the central nervous system (CNS), are crucial for maintaining the function and integrity of axons and myelin sheaths. In demyelination pathologies, various factors hinder the normal differentiation of oligodendrocyte precursor cells, obstructing the myelin regeneration process, which is a primary barrier to therapeutic myelin repair. Emerging evidence highlights the critical role of glial cell interactions in CNS homeostasis and myelin regeneration, increasing interest in the treatment of demyelinating diseases. This article reviews the role of interactions between oligodendrocytes and other CNS glial cells in demyelinating and neurological diseases. Previous findings suggest that other CNS glial cells influence the survival and metabolic activity of oligodendrocytes through cell interactions, significantly affecting myelin formation and impacting demyelinating diseases characterized by myelin regeneration disorders. Targeted modulation of oligodendrocytes and their interactions with other cells at specific temporal stages may indicate a novel therapeutic direction for demyelinating diseases and offer fresh perspectives on the study of mechanisms and therapeutic approaches for related neurological conditions.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2026046
Epstein-Barr virus-associated gastric cancer (EBVaGC) displays unique clinicopathological hallmarks, yet serology-based tools for its detection are still limited. Here, we develop a functional EBV proteome microarray covering 72 viral proteins and apply it to profile antibody responses in 62 gastric cancer patients. The resulting landscape reveals an IgG-skewed humoral signature specific to EBVaGC and identifies 34 EBV antigens exhibiting differential reactivities. Multivariable logistic regression integrates complementary markers into an optimal five-analyte panel (LF2_IgG, BBLF2_IgG, BLRF2_IgG, BPLF1-2_IgA, and BGLF4_IgA) that achieves outstanding discrimination performance (AUC = 0.93) in an independent validation set (n = 316). The panel’s performance is further validated in a community-based screening cohort (n = 474), where it achieves 87.3% sensitivity and 88.3% specificity for distinguishing EBVaGC from non-malignant gastric conditions spanning gastritis to dysplasia (AUC = 0.94). Together, these results establish a serological framework for EBVaGC diagnosis and provide a scalable strategy for population-level screening that could materially improve the management of this virus-driven malignancy.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2026080
DNAJC9, an HSP40 family member with histone chaperone function, exhibits unclear roles in cervical cancer. DNAJC9 is specifically overexpressed in malignant cervical cancer cells, and downregulation of DNAJC9 inhibits proliferation, induces G1/S arrest, and suppresses tumorigenicity. GLI1 has been identified as a key downstream effector of DNAJC9, and GLI1 rescue reverses proliferation defects. Mechanistically, DNAJC9 promotes the p300-H3 interaction to sustain H3K27ac at the GLI1 enhancer and facilitate GLI1 transcription, driving proliferation. Furthermore, DNAJC9 expression correlates positively with GLI1 in clinical specimens, suggesting that the DNAJC9-GLI1 axis is a potential prognostic marker and therapeutic target.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025105
Demyelinating diseases of the central nervous system (CNS) are characterized by failed remyelination, largely due to arrested oligodendrocyte precursor cell (OPC) differentiation. This review synthesizes evidence on the crosstalk between oligodendrocytes (OLGs) and other glial cells—astrocytes, microglia, and neurons—in the context of demyelination. OLGs, the myelin-forming cells of the CNS, are essential for axonal integrity and saltatory conduction. Under pathological conditions, factors including astrocyte-derived PDGF and leukemia inhibitory factor (LIF), microglial polarization states, and neuronal activity modulate OLG survival, metabolic support, and process outgrowth. Astrocytes promote process outgrowth via basic fibroblast growth factor (bFGF) and extracellular matrix interactions, while also regulating iron metabolism and exosomal secretion from OPCs through integrin β4-mediated adhesion. Microglial heterogeneity, with M1/M2 polarization, influences neuroinflammation and remyelination outcomes. The review highlights that astrocyte activation via STAT3 signaling determines the balance between oligodendrocyte and Schwann cell remyelination. These intercellular interactions significantly impact myelin regeneration and offer potential therapeutic targets. Modulating these interactions at specific temporal stages may provide novel strategies for treating demyelinating diseases and related neurological conditions. The integration of single-cell resolution data on microglial heterogeneity and spatial-temporal dynamics is critical for developing targeted interventions.