Frontiers in Cell and Developmental Biology最新文献

{"title":"Autophagy: mechanisms, roles in human diseases, and therapeutic perspectives.","authors":"Jiazhen He, Teng Qi","doi":"10.3389/fcell.2026.1776289","DOIUrl":"https://doi.org/10.3389/fcell.2026.1776289","url":null,"abstract":"<p><p>Autophagy, a conserved intracellular degradation and recycling process, maintains cellular homeostasis by eliminating damaged organelles, misfolded proteins, and invading pathogens. Dysregulation of autophagy either excessive or insufficient contributes to the pathogenesis of numerous human diseases, spanning the respiratory, locomotor, circulatory, digestive, urinary, and nervous systems, as well as cancer. This Mini Review summarizes the core mechanisms and classification of autophagy, highlights its dual roles in various pathological conditions, discusses existing controversies and research gaps, and outlines potential future directions for therapeutic targeting. A concise overview of key findings provides readers with an updated understanding of autophagy's multifaceted functions in disease development and treatment.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1776289"},"PeriodicalIF":4.6,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13125100/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147813210","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":"From organelles to therapy: rethinking combined hepatocellular-cholangiocarcinoma.","authors":"Tiezhong Zhang, Kangshuai Li, Qi Li, Qiang Gao, Lixin Du, Jian Deng, Zhuohan Cao, Sen Guo, Zongli Zhang","doi":"10.3389/fcell.2026.1787784","DOIUrl":"https://doi.org/10.3389/fcell.2026.1787784","url":null,"abstract":"<p><p>Combined hepatocellular-cholangiocarcinoma (cHCC-CCA) is a rare primary malignant hepatic neoplasm, defined by the concurrent presence of hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA) components, which vary in proportion and degree of differentiation. Characterized by insidious onset, high invasiveness, and marked heterogeneity, cHCC-CCA often eludes early diagnosis, leading to a generally dismal prognosis. Its survival outcomes typically fall between those of HCC and intrahepatic cholangiocarcinoma (iCCA). Epidemiological data derived from surgical resection specimens and percutaneous biopsy samples indicate that cHCC-CCA accounts for approximately 0.4%-14.2% of all primary liver cancers. Due to its rarity, standardized treatment protocols are currently lacking. Surgical resection and liver transplantation are considered the primary potential curative approaches. However, only a minority of patients meet surgical criteria at diagnosis, and postoperative recurrence rates are substantially high. For non-surgical candidates, local or systemic therapies are generally administered based on treatment regimens for HCC or iCCA. Additionally, the pronounced genetic and molecular heterogeneity of cHCC-CCA significantly compromises the efficacy of current therapeutic strategies. Its unique biological behaviors, histological features, and immunophenotypic profiles present multifaceted challenges to diagnosis, treatment, and research endeavors. This review aims to comprehensively synthesize the classification systems and pathological characteristics of cHCC-CCA, with a particular focus on the underlying organelle dysfunction. By integrating advances in clinical diagnosis and management, we seek to enhance disease awareness and provide a new reference for clinical practice.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1787784"},"PeriodicalIF":4.6,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13124961/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147813148","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":"Orchestrating innate immunity through RNA editing and helicase activity: ADAR1, dsRNA sensors, and tumor immune evasion.","authors":"Moeko Minakuchi, Joseph M Salvino, Jessie Villanueva","doi":"10.3389/fcell.2026.1788799","DOIUrl":"https://doi.org/10.3389/fcell.2026.1788799","url":null,"abstract":"<p><p>Dysregulated dsRNA editing and RNA metabolism in cancer contribute to immune evasion, highlighting the critical role of RNA structural regulation in disease. Intracellular RNA structures regulate gene expression, innate immunity, genome stability, and cell fate. Among these, double-stranded RNA (dsRNA) is particularly important; exogenous dsRNA typically originates from viral infection, whereas endogenous dsRNA arises from repetitive elements or transcriptional errors, allowing cells to distinguish \"self\" from \"non-self.\" The RNA-editing enzyme Adenosine Deaminase Acting on RNA 1 (ADAR1) prevents inappropriate innate immune activation by catalyzing adenosine-to-inosine (A-to-I) editing of endogenous dsRNA. RNA helicases complement this function by remodeling RNA structures and resolving nucleic acid hybrids, maintaining RNA homeostasis and immune surveillance. Recent studies have revealed an interplay between ADAR1 and RNA helicases that regulate dsRNA immunogenicity and R-loop dynamics, establishing this network as a key determinant of tumor immunity. Dysregulated RNA editing and structural regulation in cancer further underscore the potential of targeting these pathways therapeutically, providing strategies beyond conventional gene- or protein-centered approaches. In this review, we summarize current insights into how ADAR1 and RNA helicases control RNA structure, emphasize their roles in innate immune sensing, and discuss emerging approaches to modulate RNA editing and RNA architecture for therapeutic benefit. Taken together, research in this area positions RNA structural control as a central determinant of immune homeostasis and a promising frontier in cancer therapy.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1788799"},"PeriodicalIF":4.6,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13121243/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147767374","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":"Bridging science and hope: the evolving story of gene therapy for neuromuscular diseases.","authors":"Nicolas Wein, Florian Barthélémy","doi":"10.3389/fcell.2026.1765367","DOIUrl":"https://doi.org/10.3389/fcell.2026.1765367","url":null,"abstract":"<p><p>The field of gene therapy for neuromuscular dystrophies has evolved over the past two decades. Despite some outstanding positive outcomes, some unfortunate adverse effects also led to big setbacks. One important key point is to study relevant preclinical models and to embrace diverse strategies to mitigate or avoid such negative outcomes. Although at first, for some diseases, the promise of a one-treatment-for-all approach was envisioned, it has recently become clear that a personalized approach will likely be preferable given the high variability in response between individuals.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1765367"},"PeriodicalIF":4.6,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13121298/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147767219","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":"Integrative single-cell and bulk RNA sequencing unravels the role of ACTN1 in promoting lung cancer with brain metastasis and epidermal growth factor receptor-tyrosine kinase inhibitor resistance.","authors":"Wentian Wu, Min Yang, Jiaxuan Qin, Shangjia Gui, Ziyu Zhang, Yiruo Zhang, Yingying Du","doi":"10.3389/fcell.2026.1738641","DOIUrl":"https://doi.org/10.3389/fcell.2026.1738641","url":null,"abstract":"<p><strong>Background: </strong>Brain metastasis (BM) remains a severe and fatal complication in patients with lung cancer (LC), presenting a major therapeutic challenge. Although epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) have emerged as a cornerstone of targeted therapy, their clinical efficacy is often limited by the inevitable development of drug resistance.</p><p><strong>Methods: </strong>We initially constructed a general atlas of the tumor microenvironment (TME) in LCBM lesions by integrating single-cell RNA sequencing (scRNA-seq) data. The sensitivity of each cell cluster to EGFR-TKIs was assessed by the \"Beyondcell\" method. By performing high-dimensional Weighted Gene Co-expression Network Analysis (hdWGCNA), we identified hub genes within an EGFR-TKI resistance-associated cell cluster. Finally, the functional role of the most promising candidate, ACTN1, was further investigated in a constructed osimertinib-resistant LC cell line.</p><p><strong>Results: </strong>We identified a malignant and therapy-resistant ACTN1⁺ epithelial cell subcluster. Both signaling and functional enrichment analyses demonstrated marked activation of PI3K-Akt and IL-17 signaling pathways in ACTN1-high patient subgroups. Finally, we applied machine learning methods to the ACTN1-related genes to select prognostic factors. <i>In vitro</i> experiments confirmed the pro-resistance and pro-metastatic functions of ACTN1 in osimertinib-resistant LC cells.</p><p><strong>Conclusion: </strong>ACTN1 was discovered to induce malignant progression and formation of EGFR-TKI resistance. Targeting ACTN1-related pathways may provide novel insights to treat LCBM and overcome intracranial EGFR-TKI resistance.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1738641"},"PeriodicalIF":4.6,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13122775/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147767412","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":"Evolutionary pathway and genetic mechanisms of fin-to-limb transition in vertebrates.","authors":"Andrey V Bayramov, Dmitry N Mednikov, Andrey G Zaraisky","doi":"10.3389/fcell.2026.1784849","DOIUrl":"https://doi.org/10.3389/fcell.2026.1784849","url":null,"abstract":"<p><p>The transformation of paired appendage structure from aquatic fins to terrestrial limbs represents a pivotal event in vertebrate evolution, underpinning the colonization of land by early tetrapods. This transition involved profound morphological and genetic modifications, particularly in the distal limb region known as the autopod and in the dorsoventral plane of paired appendages. Recent advances in paleontology, comparative and functional genomics, as well as evo-devo studies have shed light on several key events and evolutionary pathways and have improved our understanding of the direction of changes in regulatory mechanisms underlying the fin-to-limb transition. In this review, we aim to summarize current knowledge on limb evolution, with particular emphasis on studies of phylogenetically pivotal vertebrate groups - cartilaginous fishes and chondrosteans, which represent basally diverging evolutionary lineages of extant vertebrates, as well as sarcopterygians, the group of lobe-finned fishes most closely related to tetrapods. We consider the principal hypotheses concerning the prerequisites for vertebrate terrestrialization, key aspects in the search for structural homology between the morphological elements of fins and limbs, as well as the genetic mechanisms of spatial limb bud development described to date and the possible modifications of these mechanisms associated with the transformation of ancestral fins into pentadactyl terrestrial limbs.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1784849"},"PeriodicalIF":4.6,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13121165/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147767268","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":"PC3/Tis21/BTG2 and BTG1 genes: regulators of the cell cycle and neurogenesis, as well as tumor suppressors in malignant brain tumors.","authors":"Manuela Ceccarelli, Laura Micheli, Giorgio D'Andrea, Felice Tirone","doi":"10.3389/fcell.2026.1775035","DOIUrl":"https://doi.org/10.3389/fcell.2026.1775035","url":null,"abstract":"<p><p><i>PC3/Tis21/BTG2</i> and <i>BTG1</i>, prototype members of the <i>BTG</i>/<i>Tob</i> family, are antiproliferative transcriptional cofactors discovered 35 years ago as genes induced by nerve growth factor and phorbol 12-myristate 13-acetate or associated with lymphocytic leukemia. They are today known to serve as developmental regulators in several tissues, including neural cells. Biological functions such as cell division, transcriptional control, DNA repair, and mRNA stability, have been linked to their protein products. We will focus in this review on the effects of <i>PC3</i>/<i>Tis21</i>/<i>BTG2</i> and <i>BTG1</i> on brain tumorigenesis and neural development, and on cell cycle and apoptosis. In fact, these genes act as tumor suppressors, and their ability to control tumorigenesis in medulloblastoma and glioma is intrinsically linked to their ability to control the differentiation and proliferation of neural stem and progenitor cells during neurogenesis. Chief function of <i>PC3</i>/<i>Tis21</i>/<i>BTG2</i> during pre/postnatal and adult neurogenesis is its requirement for the differentiation and migration of neural progenitor cells, in adult hippocampus and subventricular zone-which are the main neurogenic niches where adult neurogenesis occurs-as well as in postnatal cerebellum. Moreover, <i>PC3</i>/<i>Tis21</i>/<i>BTG2</i> inhibits medulloblastoma onset by promoting the migration and differentiation of cerebellar precursor cells outside the external granular layer, i.e., the proliferative epithelium of the cerebellum, thus diminishing their susceptibility to oncogenic transformation under the influence of Sonic Hedgehog. <i>BTG1</i>, by contrast, primarily functions in neurogenesis to inhibit the proliferation of neural stem and progenitor cells, thereby ensuring the preservation of the cell pool and maintaining the quiescence of medulloblastoma cancer stem cells-known for their persistence against treatments and involvement in tumor relapses-thus preventing their entry in cycle. Furthermore, in glioma, <i>PC3</i>/<i>Tis21</i>/<i>BTG2</i> enhances apoptosis rates while simultaneously decreasing the migration and invasion of cancerous cells, and lowering the levels of <i>cyclin D1</i>. Similarly, <i>BTG1</i> contributes to the growth arrest of glioma cells through the regulation of <i>cyclin D1</i> and <i>p21</i> expression. <i>PC3/Tis21</i>/<i>BTG2</i> and BTG1 bind and regulate multiple genes, including <i>Id3</i>, <i>cyclin D1</i>, <i>PRMT1</i> and the chemokine <i>Cxcl3</i>. These interactions underscore the potential of these cofactors in controlling neurogenesis and tumorigenesis through multiple molecular pathways.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1775035"},"PeriodicalIF":4.6,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13133959/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147813176","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":"G-patch proteins: important regulators of pre-mRNA splicing and ribosome biogenesis.","authors":"Laura Olivia Karika, Ingrid Cipakova, Lucia Hronska, Lubos Cipak","doi":"10.3389/fcell.2026.1750689","DOIUrl":"https://doi.org/10.3389/fcell.2026.1750689","url":null,"abstract":"<p><p>Pre-mRNA splicing is a fundamental step in eukaryotic gene expression, carried out by the spliceosome. This large and dynamic ribonucleoprotein complex undergoes extensive structural rearrangements during each splicing event. Similarly, ribosome biogenesis is a highly regulated process that requires precise control at every stage, from the transcription of pre-rRNA through its chemical modification and cleavage to the final assembly of mature ribosomal subunits. Central to the regulation of both pre-mRNA splicing and ribosome biogenesis are RNA helicases and their cofactors, notably G-patch proteins. The predominance of G-patch proteins in eukaryotes underscores their evolutionary importance in the increasing complexity of RNA processing and ribosome biogenesis. This review summarizes recent findings on the molecular functions and regulatory roles of various G-patch proteins in the yeasts <i>S. cerevisiae</i> and <i>S. pombe</i>, as well as in humans. Growing evidence indicates that these proteins act as critical cofactors of RNA helicases involved in splicing, facilitating the dynamic transitions required for spliceosome activation, catalysis, and disassembly. Beyond splicing, these proteins also contribute to the regulation of ribosome biogenesis and other aspects of RNA metabolism. Dysregulation or mutation of G-patch proteins have been shown to cause aberrant mRNA maturation, altered splicing patterns, impaired ribosome assembly, and genomic instability. Such perturbations are associated with a range of human diseases, including cancer progression. Despite the essential roles of G-patch proteins in regulating pre-mRNA splicing and ribosome biogenesis, the precise molecular functions and interaction networks of many G-patch proteins remain poorly understood. Future studies aimed at elucidating the mechanisms by which these proteins coordinate RNA processing and ribosome biogenesis are therefore essential. Such investigations may help uncover the molecular basis of G-patch protein-associated diseases and reveal new potential targets for therapeutic intervention.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1750689"},"PeriodicalIF":4.6,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13111387/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147767359","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":"Metabolic reprogramming in intervertebral disc degeneration: mechanisms and therapeutic opportunities.","authors":"Qing Lu, Caiyou He","doi":"10.3389/fcell.2026.1811737","DOIUrl":"https://doi.org/10.3389/fcell.2026.1811737","url":null,"abstract":"<p><p>Intervertebral disc degeneration (IVDD) is a major cause of chronic low back pain and disability and imposes a substantial socioeconomic burden. Increasing evidence indicates that metabolic reprogramming is closely involved in the initiation and progression of IVDD. In this review, we summarize the major pathological processes associated with IVDD, including apoptosis, autophagy dysregulation, oxidative stress, inflammatory responses, and extracellular matrix (ECM) degradation. We further discuss alterations in glucose, lipid, and amino acid metabolism, with particular emphasis on the contribution of mitochondrial dysfunction to metabolic imbalance in disc cells. In addition, we outline the genetic, environmental, and signaling factors that regulate metabolic reprogramming, including pathways such as mTOR and AMPK. Finally, we review emerging metabolism-related therapeutic strategies, including metabolic enzyme modulation, antioxidants, and mitochondrial protectors. Collectively, current evidence suggests that metabolic reprogramming is an important component of IVDD pathogenesis and may provide a useful framework for the development of targeted therapeutic approaches.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1811737"},"PeriodicalIF":4.6,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13111279/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147767384","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":"An animal component-free bioprocess for synthesizing 3D human matrix scaffolds using mesenchymal stromal cells.","authors":"Shaianne N Stein, Lorena R Braid","doi":"10.3389/fcell.2026.1624745","DOIUrl":"https://doi.org/10.3389/fcell.2026.1624745","url":null,"abstract":"<p><strong>Introduction: </strong>The basement membrane is a specialized extracellular matrix that compartmentalizes epithelial and endothelial tissues and provides essential structural and signaling cues for tissue organization. Whereas fibrillar collagens (Col) of the interstitial matrix (such as Col I and Col III) are widely used in tissue modeling, the networking collagens that scaffold the basement membrane, including human Col IV and Col VI, remain difficult to access. Commercial basement membrane surrogates such as Matrigel® are derived from murine tumors and are ill defined, dilute, variable, and incompatible with animal-free biomanufacturing. Thus, there is a crucial need for human-derived basement membrane matrices that are free of xenogenic contaminants and do not rely on breeding animals.</p><p><strong>Methods: </strong>Here, we analyzed whether human mesenchymal stromal cells (MSCs) could serve as a platform to produce self-assembling basement membrane components under chemically defined, xeno-free conditions. MSCs from placental, umbilical cord, bone marrow, and adipose tissues were cultured as three-dimensional spheroids and adherent multilayered sheets.</p><p><strong>Results: </strong>Confocal imaging of whole-mount, decellularized spheroid matrices showed complex networks of fibronectin (FN) and Col IV with topological and organizational features characteristic of basement membrane. Perinatal MSCs produced distinct matrix architectures consisting of apical FN sheets underlaid by continuous Col IV networks. Time-resolved imaging of umbilical cord MSC-derived matrix sheets demonstrated a reproducible sequence of basement membrane assembly that parallels developmental tissue organization.</p><p><strong>Discussion: </strong>Together, these findings demonstrate that human MSCs cultured entirely without entirely animal-derived components can synthesize functional basement membrane proteins that self-assemble into ordered, tissue-like scaffolds. In this work, we establish MSCs as a scalable, sustainable, and cruelty-free platform for manufacturing human basement membrane matrices for bioengineering and regenerative medicine applications.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1624745"},"PeriodicalIF":4.6,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13111481/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147767250","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}