Frontiers in Cell and Developmental Biology最新文献

{"title":"Differential regulation of gene co-expression modules in muscles and liver of preterm newborns.","authors":"Petra Janovska, Tatyana Kobets, Lenka Steiner Mrazova, Michaela Svobodova, Marketa Tesarova, Pavel Kopecky, Petr Zouhar, Martin Rossmeisl, Viktor Stranecky, Stanislav Kmoch, Jan Kopecky","doi":"10.3389/fcell.2025.1645959","DOIUrl":"https://doi.org/10.3389/fcell.2025.1645959","url":null,"abstract":"<p><strong>Background: </strong>Newborns undergo rapid metabolic and organ adaptations after birth, which are compromised in premature newborns, leading to adverse health outcomes. Molecular mechanisms underlying these transitions remain poorly understood due to limited tissue availability. To address this gap, we characterized tissue transcriptomes using autopsy samples from a unique newborn cohort.</p><p><strong>Methods: </strong>We analyzed liver (LI), heart (HM), and skeletal muscle (SM) transcriptomes using RNA sequencing in 41 predominantly premature newborns who died shortly after birth. Nearly 14,000 protein-coding gene transcripts per tissue were detected.</p><p><strong>Results: </strong>Tissues exhibited distinct expression profiles, with LI showed the highest number of tissue-specific genes. SM gene expression correlated strongly with gestational age at birth (i.e., the prenatal development), while LI was influenced by the duration of postnatal survival (i.e., the postnatal development). HM displayed minimal changes, suggesting stable myocardial metabolism during the perinatal transition. Weighted Gene Co-expression Network Analysis (WGCNA) identified tissue-specific gene co-expression modules linked to clinical traits such as gestational age, birth weight, survival duration, nutrition, and exposure to catecholamine treatment. The key functional annotations, validated by differential expression analysis, revealed that LI and SM modules were enriched for mitochondrial metabolism and oxidative phosphorylation genes, with more pronounced prenatal development in SM, and a postnatal increase in both tissues. Data suggests that energy metabolism in SM matures first, followed by the development of muscle functions. Hepatic modules were associated with a postnatal increase in the steroid hormone/xenobiotic metabolism, and a decline in hematopoietic activity. Robust annotations to ribosome activity suggested tissue-specific changes in protein synthesis, which declined prenatally in SM, postnatally in HM. Notably, the supply of exogenous glucose and nutrition type were strongly associated with hepatic gene expression, highlighting the central role of the liver in postnatal metabolic adaptation.</p><p><strong>Conclusion: </strong>Overall, our study highlights tissue-specific perinatal gene regulation, with mitochondrial maturation emerging as a crucial driver of postnatal adaptation, explaining vulnerabilities in preterm infants. We provide a unique resource for characterizing developmental changes in tissue transcriptomes during the fetal-to-neonatal transition in human newborns.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1645959"},"PeriodicalIF":4.6,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12518348/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145298943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Non-histone lactylation: unveiling its functional significance.","authors":"Pusong Shi, Yongjie Ma, Shaolu Zhang","doi":"10.3389/fcell.2025.1707124","DOIUrl":"https://doi.org/10.3389/fcell.2025.1707124","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3389/fcell.2025.1535611.].</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1707124"},"PeriodicalIF":4.6,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12519453/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145299660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in precision oncology using patient-derived organoids and functional biomaterials.","authors":"Hina Singh, Ivan Mijakovic, Priyanka Singh","doi":"10.3389/fcell.2025.1670328","DOIUrl":"https://doi.org/10.3389/fcell.2025.1670328","url":null,"abstract":"<p><p>Despite major advances in oncology, cancer therapy continues to face persistent challenges due to intratumoral heterogeneity, drug resistance, and the poor clinical translation of experimental therapeutics. Conventional preclinical models such as 2D cultures and animal systems often fail to accurately recapitulate the tumor microenvironment immune contexture, and patient-specific variability limiting their predictive power. While nanomedicine and advanced drug delivery platforms offer promising solutions, their translational success is hindered by insufficient integration with physiologically relevant tumor models. In this review, we critically examine how patient-derived organoids derived from patient tumors serve as next-generation platforms for modeling cancer heterogeneity, therapeutic response, and biomarker discovery. We further explore how the integration of PDOs with functional biomaterials, extracellular matrix mimetics, and organ-on-chip systems enables dynamic co-culture environments that capture tumor-stroma-immune interactions with high fidelity. By linking the biological underpinnings of resistance, such as genetic mutations, altered signaling, metabolic rewiring, and immune evasion, with smart biomaterial design and drug screening workflows, we propose a unified roadmap for precision oncology. Additionally, we highlight the emergence of PDO biobanks, co-culture innovations, and high-throughput phenotypic screening as essential tools for improving clinical translation. This interdisciplinary synthesis underscores the transformative potential of PDO-based platforms in accelerating personalized cancer therapy.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1670328"},"PeriodicalIF":4.6,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12518345/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145299601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retinoids in scarless skin regeneration: from molecular mechanisms to therapeutic strategies.","authors":"Kang Wang, Ziting Yang, Yunqi Ma, Wenhui Liu, Guangshuai Li, Xuewen Xu, Qingfeng Li","doi":"10.3389/fcell.2025.1683851","DOIUrl":"https://doi.org/10.3389/fcell.2025.1683851","url":null,"abstract":"<p><p>Scarless skin regeneration remains one of the most ambitious goals in regenerative medicine. Unlike fibrotic healing, which results in excessive collagen accumulation and functional impairment, true regeneration restores both the structural integrity and physiological function of skin, including the reconstitution of hair follicles and other appendages. Retinoids, a broad class of natural and synthetic vitamin A derivatives, have attracted increasing attention for their potential to modulate wound repair at multiple levels. These compounds regulate a diverse array of biological processes, including epidermal differentiation, fibroblast activation, immune response, and extracellular matrix remodeling. This review provides a comprehensive overview of how retinoids coordinate cellular and molecular events across key skin compartments during healing. Retinoids have been reported to suppress TGF-β1/Smad signaling, inhibit myofibroblast differentiation, and restore matrix homeostasis, thereby exerting anti-fibrotic effects. In addition, retinoid-based therapies enhance re-epithelialization, stimulate angiogenesis, and promote dermal regeneration when incorporated into advanced biomaterial systems. Recent studies further demonstrate that retinoids can support skin appendage regeneration, including <i>de novo</i> hair follicle formation, a hallmark of functional repair typically absent in adult wounds. In view of converging evidence from developmental biology, stem cell research, and regenerative engineering, retinoids present a promising pharmacological strategy in reduced-scarring healing and functional skin regeneration.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1683851"},"PeriodicalIF":4.6,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12515861/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145291688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell and bulk RNA-sequencing reveal PRRX2-driven cancer-associated fibroblast-mediated perineural invasion for predicting the immunotherapy outcome in colorectal cancer.","authors":"Mingxiao Chen, Yue Cai, Feng Han, Bo Li, Zhou Xu, Kaili Cui, Wenqi Bai, Feng Li","doi":"10.3389/fcell.2025.1620388","DOIUrl":"https://doi.org/10.3389/fcell.2025.1620388","url":null,"abstract":"<p><strong>Background: </strong>Perineural invasion (PNI) is common in a variety of solid tumors and has been identified as an important pathway promoting tumor local invasion and distant metastasis. Its presence is usually associated with increased aggressiveness, malignant biology, and a worse patient prognosis. However, its specific role and regulatory mechanisms in colorectal cancer (CRC) remain unclear.</p><p><strong>Methods: </strong>In this study, we integrated 20 CRC single-cell transcriptome datasets, which contained 575,768 high-quality cells, and used the Scissor algorithm to map PNI phenotypes in TCGA bulk samples to the single-cell level. Nine cancer-associated fibroblast (CAF) subpopulations were identified and functionally annotated. We evaluated the clinical relevance of CAF subsets in TCGA and three independent cohorts (silu_2022, GSE39582, and GSE17536) using BayesPrism-based deconvolution. We analyzed transcriptional regulatory networks using pySCENIC and validated PRRX2 function by <i>in vitro</i> experiments. Immune infiltration characteristics were quantified using the ssGSEA score, and the association between the PRRX2 score and immune checkpoint inhibitor efficacy was analyzed in conjunction with two immunotherapy cohorts. In addition, we performed a drug sensitivity analysis based on the GDSC pharmacogenomics database to screen potential therapeutic agents.</p><p><strong>Results: </strong>In this study, we systematically revealed the characteristics of the perineural invasion-associated fibroblast subsets and their regulatory mechanisms. In PNI-positive tumors, the proportion of fibroblasts was significantly increased, with the enrichment of MMP2+ myofibroblastic cancer-associated fibroblasts (myCAFs), and facilitated perineural infiltration through extracellular matrix remodeling. Further analysis revealed that PRRX2 was a core regulator of MMP2+myCAFs, promoting perineural invasion through the activation of TGF-β signaling pathways. PRRX2 knockdown significantly inhibited fibroblast proliferation, clonogenic formation, and invasive migration capacity, and it reduced TGFB1 and NGF expressions. The clinical cohort validation demonstrated a significant correlation between the PRRX2-score and advanced tumor stage, along with vascular and lympho-vascular invasion (LVI). Furthermore, patients with high PRRX2 scores had a significantly worse prognosis. In addition, patients with high PRRX2 scores responded poorly to immune checkpoint inhibitors but may be sensitive to targeted agents or antibody-coupled drugs, which may serve as potential targets for combination therapy.</p><p><strong>Conclusion: </strong>This analysis established PRRX2-driven MMP2+myCAFs as pivotal mediators of CRC perineural invasion through TGF-β/ECM remodeling. The PRRX2 score serves as a biomarker for prognosis prediction and immunotherapy outcome.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1620388"},"PeriodicalIF":4.6,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12516196/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145291616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in mild photothermal hydrogel-based therapies for bone and soft tissue injuries.","authors":"Peng Na, Jing-Lun Jiang, Ren-Peng Lv, Fan Yang, Shi-Feng Li, Xian-Zhuo Chen","doi":"10.3389/fcell.2025.1696209","DOIUrl":"10.3389/fcell.2025.1696209","url":null,"abstract":"<p><p>Bone and soft tissue injuries resulting from trauma, metabolic disorders, and tumors pose a serious threat to public health, and their treatment faces numerous challenges, including infection, chronic inflammation, and impaired vascularization. Photothermal hydrogels, a new class of biomaterials, can sterilize tissues via photothermal therapy (PTT) and, through intelligent material design, exhibit multiple biological functions such as modulating the pathological microenvironment in bone and soft tissues. These properties have earned them a reputation as a \"star material\" in tissue engineering. However, excessive heating (above 50 °C) can cause irreversible thermal damage to tissues. Therefore, functional hydrogels that generate a mild photothermal effect (approximately 40 °C-45 °C) have recently become a research focus. This review provides a comprehensive overview of the types and fabrication strategies of photothermal agents used in mild photothermal hydrogels, systematically summarizes recent progress in their applications for bone and soft tissue injury repair, and delves into the underlying mechanisms by which they promote tissue regeneration. By summarizing current findings and outlining future perspectives on the use of mild photothermal hydrogels in modern regenerative medicine, we aim to advance the development of tissue engineering.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1696209"},"PeriodicalIF":4.6,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511113/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145279344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Involvement of <i>ACSM</i> family genes in the reprogramming of lipid metabolism within tumors and their investigation as promising therapeutic targets.","authors":"Ke-Xin Fang, Zi-Qi Li, Jin-Liang Dong, Ze Yu","doi":"10.3389/fcell.2025.1663033","DOIUrl":"10.3389/fcell.2025.1663033","url":null,"abstract":"<p><p>Metabolic reprogramming of tumor cells is an important feature of oncogenesis and progression, with lipid metabolism playing a key role in this process. The enzymes encoded by the ACSM (Acyl-CoA Synthetase Medium-Chain Family) genes play a crucial role in fatty acid activation, affecting the energy supply and membrane synthesis of tumor cells. In recent years, research on the expression patterns of ACSM family genes in different tumor types and their regulatory mechanisms has gradually increased, revealing their close relationship with tumor development. However, current research on ACSM family genes still has some shortcomings, such as a lack of systematic large-scale clinical data support and an in-depth understanding of their regulatory networks. This work summarizes the role of ACSMs in tumor lipid metabolic reprogramming and explores their research progress as potential therapeutic targets, providing new ideas for future tumor treatment.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1663033"},"PeriodicalIF":4.6,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511025/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145279433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A comparative transcriptomics analysis of mammalian and non-mammalian acute kidney injury (AKI) models.","authors":"Matthew R Hawkins, Diana Cervera, Tiffany M Tang, Rebecca A Wingert","doi":"10.3389/fcell.2025.1653967","DOIUrl":"10.3389/fcell.2025.1653967","url":null,"abstract":"<p><strong>Introduction: </strong>Acute kidney injury (AKI) is a complex clinical condition characterized by decline in renal function and widespread transcriptional dysregulation. While transcriptomic studies that compare human and other mammalian models of AKI have provided insight, much less is known about commonalities and contrasts between mammalian models and nontraditional and regenerative laboratory models. Understanding these molecular level responses to injury in both regenerative and non-regenerative models may reveal conserved and unique pathways in renal repair.</p><p><strong>Methods: </strong>To investigate transcriptional responses to AKI across species, we incorporated newly available RNA-seq data from zebrafish, axolotl, and spiny mouse models into an expanded cross-species comparative analysis. These were analyzed alongside existing and previously analyzed data from both human and mouse (Mus) models. Differential gene expression and gene-ontology (GO) enrichment analyses we utilized to identify conserved and regeneration-specific during injury and recovery phases.</p><p><strong>Results: </strong>Comparative transcriptomic analysis revealed distinct transcriptional programs in each species during AKI, including both shared and species-specific responses. Of note, zebrafish show differential expression of apolipoproteins, molecules of increasing interest to the greater field of nephrology. In the recovery setting, we show that animals with regenerative capacity have conserved and divergent transcriptional programs.</p><p><strong>Discussion: </strong>Our findings demonstrate that non-traditional animal models of AKI, such as zebrafish, axolotls, and spiny mice, provide valuable insights into the molecular basis of kidney regeneration. The identification of conserved and divergent injury responses suggests evolutionary conservation in core AKI mechanisms, while also pointing to regeneration-associated transcriptional programs that could inform future therapeutic strategies. This work underscores the importance of using non-traditional models as well as the value in comparative analysis with traditional models and clinical data.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1653967"},"PeriodicalIF":4.6,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12510925/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145279371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modeling craniofacial spliceosomopathies: a pathway toward deciphering disease mechanisms.","authors":"Casey Griffin","doi":"10.3389/fcell.2025.1624043","DOIUrl":"10.3389/fcell.2025.1624043","url":null,"abstract":"<p><p>Craniofacial spliceosomopathies are syndromes resulting from mutations in components of the spliceosome, presenting with facial dysostosis in combination with other phenotypes. An outstanding question in the field is how mutations in the ubiquitously expressed spliceosome lead to such cell- and tissue-specific disorders. To understand the etiology of these diseases and decipher the underlying mechanisms, scientists have turned to modeling these disorders in the laboratory. <i>In vivo</i> modeling of these disorders includes the use of mice, zebrafish, and frogs, whereas <i>in vitro</i> modeling typically uses embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs). The goal with these models is to recapitulate the human disorders in a manner that is conducive to scientific exploration. In this review, we briefly describe the major craniofacial spliceosomopathies and discuss recent advances using model systems that have helped understand the root cause of these conditions.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1624043"},"PeriodicalIF":4.6,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12510987/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145279504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in tumor-associated macrophage-mediated chemotherapeutic resistance in glioma.","authors":"Xuebo Liu, Qi Yu","doi":"10.3389/fcell.2025.1676338","DOIUrl":"10.3389/fcell.2025.1676338","url":null,"abstract":"<p><p>Tumor-associated macrophages (TAMs) are a dominant immune component within the glioma microenvironment and are increasingly recognized as key contributors to therapeutic resistance, the major challenge in glioma management. Understanding their role is critical for developing novel therapies. This review synthesizes current knowledge on TAM-mediated chemoresistance in glioma. TAMs originate from bone marrow-derived monocytes and resident microglia, exhibiting significant heterogeneity and plasticity, particularly between pro-inflammatory (M1) and pro-tumorigenic (M2) phenotypes. M2-like TAMs drive resistance through multiple mechanisms: (1) Modulating drug metabolism/clearance (e.g., via CYP450 enzymes and P-glycoprotein); (2) Secreting protumor factors (TNF-α, ILs like IL-4/IL-6/IL-10, chemokines like CCL5/CCL22, growth factors like VEGF/EGF) that activate survival pathways, induce immunosuppression, promote angiogenesis, and enhance epithelial-mesenchymal transition (EMT); (3) Interacting with glioma stem cells (GSCs) to maintain stemness; (4) Facilitating microenvironmental adaptation (e.g., hypoxia/HIF-1α response); (5) Remodeling the extracellular matrix (ECM) via MMPs, increasing stiffness and impairing drug penetration. Targeting TAMs offers promising approaches to overcome resistance. Strategies include: (1) Reprogramming M2 to M1 phenotypes using agonists (TLR, STING, CD40) or inhibitors (STAT3/STAT6); (2) Metabolic modulation (targeting glycolysis, fatty acid oxidation, glutaminolysis); (3) Blocking recruitment axes (CCL2/CCR2, CSF-1/CSF-1R, CXCL12/CXCR4); (4) Depleting M2-TAMs (e.g., trabectedin, CAR-T cells, M2pep-drugs); (5) Enhancing phagocytosis (anti-SIRPα/CD47, anti-SIGLEC). TAMs are pivotal mediators of chemoresistance in glioma through diverse molecular and cellular mechanisms. Targeting TAM recruitment, polarization, function, or metabolism represents a promising therapeutic avenue. However, the complexity of the glioma microenvironment and blood-brain barrier necessitate combination strategies for clinical translation. Further research is needed to optimize specificity and overcome challenges like compensatory pathways and drug delivery.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"13 ","pages":"1676338"},"PeriodicalIF":4.6,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511076/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145279323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}