Cells最新文献

{"title":"The Colonic Crypt: Cellular Dynamics and Signaling Pathways in Homeostasis and Cancer.","authors":"Anh L Nguyen, Molly A Lausten, Bruce M Boman","doi":"10.3390/cells14181428","DOIUrl":"10.3390/cells14181428","url":null,"abstract":"<p><p>The goal of this review is to expand our understanding of how the cellular organization of the normal colonic crypt is maintained and elucidate how this intricate architecture is disrupted during tumorigenesis. Additionally, it will focus on implications for new therapeutic strategies targeting Epithelial-Mesenchymal Transition (EMT). The colonic crypt is a highly structured epithelial unit that functions in maintaining homeostasis through a complex physiological function of diverse cell types: SCs, transit-amplifying (TA) progenitors, goblet cells, absorptive colonocytes, Paneth-like cells, M cells, tuft cells, and enteroendocrine cells. These cellular subpopulations are spatially organized and regulated by multiple crucial signaling pathways, including WNT, Notch, Bone Morphogenetic Protein (BMP), and Fibroblast Growth Factor (FGF). Specifically, we discuss how these regulatory networks control the precise locations and functions of crypt cell types that are necessary to achieve cellular organization and homeostasis in the normal colon crypt. In addition, we detail how the crypt's hierarchical structure is profoundly perturbed in colorectal cancer (CRC) development. Tumorigenesis appears to be driven by LGR5+ cancer stem cells (CSCs) and the hyperproliferation of TA cells as colonocytes undergo metabolic reprogramming. Goblet cells lose their secretory phenotype, while REG4+ Paneth-like cells foster SC niches. Tumor microenvironment is also disrupted by upregulation of M cells and by tumor-immune crosstalk that is promoted by tuft cell expansion. Moreover, the presence of enteroendocrine cells in CRC has been implicated in treatment resistance due to its contribution to tumor heterogeneity. These cellular changes are caused by the disruption of homeostasis signaling whereby: overactivation of WNT/β-catenin promotes stemness, dysregulation of Notch inhibits differentiation, suppression of BMP promotes hyperproliferation, and imbalance of FGF/WNT/BMP/NOTCH enhances cellular plasticity and invasion. Further discussion of emerging therapies targeting epithelial markers and regulatory factors, emphasizing current development in novel, precision-based approaches in CRC treatment is also included.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468274/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148228","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":"Interaction Between Human Skeletal and Mesenchymal Stem Cells Under Physioxia Enhances Cartilage Organoid Formation: A Phenotypic, Molecular, and Functional Characterization.","authors":"Cristian Mera Azain, Astrid Natalia Santamaría Durán, Tatiana Camila Castañeda, Luis Fernando Useche, Efraín Leal Garcia, Jaime Mariño Valero, Rodrigo Jaramillo Quintero, Luis Fernando Jaramillo, Jorge Andrés Franco, Rubiela Castañeda Salazar, Juan Carlos Ulloa, Ivonne Gutiérrez Rojas, Rodrigo Somoza Palacios, Claudia Cuervo Patiño, Viviana Marcela Rodríguez-Pardo","doi":"10.3390/cells14181423","DOIUrl":"10.3390/cells14181423","url":null,"abstract":"<p><p>Articular cartilage regeneration remains a major challenge due to its limited self-repair capacity. Bone marrow-derived skeletal stem cells (SSCs) and mesenchymal stem cells (MSCs) are promising candidates for cartilage engineering, although they differ in their chondrogenic potential. This study explored whether co-culturing SSCs and MSCs in three-dimensional (3D) organoid systems under cartilage physioxia (5% O₂) and chondrogenic induction could improve cartilage tissue formation. SSCs, MSCs, and SSC-MSC co-cultures were characterized for morphology, phenotype, and differentiation capacity. Organoids were generated and cultured for 10 days, followed by analysis of morphology, viability, gene expression (<i>SOX9</i>, <i>RUNX2</i>, <i>ACAN</i>, <i>COL2A1</i>, <i>COL10A1</i>, <i>PRG4</i>, and <i>PDPN</i>), chondrocyte-associated antigens (CD44, CD105, CD146, and PDPN), and cartilage ECM proteins (aggrecan, collagen types I, II, and X, and PRG4). SSCs showed robust chondrogenic and osteogenic potential, while MSCs exhibited a balanced multipotency. Co-culture-derived organoids enhanced chondrogenesis and reduced adipogenesis, with higher expression of cartilage-specific ECM and lower hypertrophic marker levels. These findings highlight the functional synergy between SSCs and MSCs in co-culture, promoting the formation of stable, cartilage-like structures under physioxia. The approach offers a promising strategy for generating preclinical models and advancing regenerative therapies for hyaline cartilage repair.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468709/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148127","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":"PA2G4 Functions as a Cofactor for MYC Family Oncoproteins in MYC-Driven Malignancies.","authors":"Sukriti Krishan, Jessica Koach, Taylor Lim, Kenny Yeo, Faith Cheong, Jie-Si Luo, Hassina Massudi, Xiaomian Gao, Sopheakwealthy Heangsarath, Andrew J Kueh, Marco J Herold, Belamy B Cheung, Glenn M Marshall","doi":"10.3390/cells14181422","DOIUrl":"10.3390/cells14181422","url":null,"abstract":"<p><p>MYCN and c-MYC are critical driver oncogenes in several childhood cancers, including neuroblastoma. Currently, the clinical development of MYC inhibitors has been hindered by the intrinsically disordered structure of MYC proteins, which lack well-defined ligand-binding pockets. Proliferation-associated protein 2G4 (PA2G4) directly binds to and stabilizes MYCN protein, leading to markedly increased MYCN levels in neuroblastoma cells. Here, we demonstrate that PA2G4 is essential for MYCN-driven tumor growth in neuroblastoma in vivo. Moreover, PA2G4 elevates c-MYC protein levels in neuroblastoma cells by inhibiting its ubiquitin-mediated degradation. In turn, c-MYC upregulates the transcription and protein expression of PA2G4, creating an oncogenic feed-forward expression loop. A small molecule PA2G4 inhibitor, WS6, directly disrupts the PA2G4-c-MYC protein-protein interaction, resulting in decreased levels of both PA2G4 and c-MYC. WS6 exhibited selective cytotoxicity in c-MYC-overexpressing cell lines. Together, these findings identify PA2G4 as a shared cofactor for both the c-MYC and MYCN oncoproteins and highlight its interaction with MYC family oncoproteins as a promising therapeutic vulnerability in MYC-driven cancers.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468391/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148196","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":"Localization and Dynamics of the Cell Shape-Determining Csd2 Protein Complex in <i>H. pylori</i>.","authors":"Maximilian Greger, Barbara Waidner","doi":"10.3390/cells14181420","DOIUrl":"10.3390/cells14181420","url":null,"abstract":"<p><p>Approximately half of the world population is infected with the human pathogen <i>Helicobacter pylori</i>, which causes gastric inflammation, chronic gastritis, or peptide ulceration. A significant factor in the colonization of the upper digestive system is the helical shape of <i>H. pylori</i>. This helical form is maintained by a complex network of peptidoglycan (PG)-modifying enzymes and cytoskeletal proteins. Among these, the D,D-endopeptidase Csd2 plays a central role, working in conjunction with other cell shape-determining (Csd) proteins. Csd1 and Csd2 have been categorized as members of the M23B metallopeptidase family. These enzymes are classified as D,D-endopeptidases, and their function involves the cleavage of the D-Ala4-mDAP3 bond, which is present in the cross-linked di-mer muropeptides. Despite the fact that the structure of the Csd1:Csd2 complex has been examined via biochemical methods, information on the in vivo localization and dynamics of D,D-endopeptidases is still missing. Here, we use an approach that employs sophisticated different microscopy methods to visualize the spatial temporal localization and dynamics of Csd2, involving both structured illumination microscopy and single-molecule tracking. Our findings thus contribute to refining the existing model for this cellular complex by revealing curvature-dependent spatial organization and temporal dynamics underlying peptidoglycan remodeling processes essential for helical cell shape formation and maintenance. Understanding the dynamics provides insight into the mechanisms that maintain bacterial morphology and potential targets for therapeutic intervention.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468929/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148086","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":"Circ-06958 Is Involved in Meat Quality by Regulating Cell Proliferation Through miR-31-5p/AK4 Axis in Pigs.","authors":"Xiaohan Zhang, Rongru Zhu, Xiaoxu Wu, Minghang Chang, Yuanlu Sun, Liang Wang, Ming Tian, Dongjie Zhang, Di Liu, Xiuqin Yang","doi":"10.3390/cells14181416","DOIUrl":"10.3390/cells14181416","url":null,"abstract":"<p><p>Circular RNA (CircRNA) can regulate gene expression through acting as a competitive endogenous RNA (ceRNA), thus becoming involved in various biological processes. However, little was known about the role of circRNA in the formation of meat quality in pigs. Here, circRNAs were first characterized in muscles with differential meat quality and myofiber composition, longissimus thoracis, and semitendinosus muscles, with RNA-sequencing (RNA-seq). A total of 1126 differentially expressed circRNAs were identified. Among them, Circ-06958 is highly expressed in both muscles. Circ-06958 originated from Long-chain acyl-CoA synthetase 1 (<i>ACSL1</i>), a gene involved in muscle development. Circ-06958 was then characterized experimentally for the first time. Next, it was revealed that Circ-06958 increased proliferation of muscle cells, including porcine skeletal muscle satellite cells (PMSCs) and C2C12 myoblasts, by promoting cell cycle progression. Circ-06958 was mainly localized in cytoplasm, indicating it can function as a ceRNA. A regulatory axis Circ-06958/miR-31-5p/Adenylate Kinase 4 (<i>AK4</i>) axis was constructed with molecular biology techniques. Afterward, it was shown that miR-31-5p inhibited cell proliferation by affecting cell cycle progression in the two cells, while <i>AK4</i> increased it. We made it clear that Circ-06958 promoted muscle cell proliferation via the miR-31-5p/<i>AK4</i> axis. The results will contribute to further revealing the mechanisms through which meat quality generates.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147950","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":"Imaging of Proteinopathies in the Brains of Parkinsonian Disorders.","authors":"Makoto Higuchi","doi":"10.3390/cells14181418","DOIUrl":"10.3390/cells14181418","url":null,"abstract":"<p><p>Neurodegenerative diseases such as Alzheimer's disease (AD), frontotemporal lobar degeneration (FTLD), and α-synucleinopathies-including Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA)-are characterized by the accumulation of misfolded protein aggregates. Advances in positron emission tomography (PET) imaging have enabled in vivo visualization of these pathologies, particularly tau and α-synuclein fibrils, facilitating early diagnosis and differential classification. Tau PET tracers such as ¹⁸F-florzolotau have demonstrated robust imaging of both AD-type and 4-repeat tauopathies, including atypical parkinsonian syndromes in FTLD such as progressive supranuclear palsy and corticobasal degeneration. Cryo-electron microscopy has elucidated the molecular interactions underlying tracer binding, highlighting hydrophobic grooves in cross-βstructures as binding components commonly present in multiple tau fibril types. For α-synucleinopathies, new tracers with a modified cross-β-binding scaffold, including ¹⁸F-SPAL-T-06 and ¹⁸F-C05-05, have shown promise in detecting MSA-related pathology and, more recently, midbrain pathology in PD and DLB. However, sensitive detection of pathologies in early PD/DLB stages remains a challenge. The integration of high-resolution PET technologies and structurally optimized ligands may enable earlier and more accurate detection of protein aggregates, supporting both clinical decision-making and the development of targeted disease-modifying therapies.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468588/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148024","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":"Multispectral Pulsed Photobiomodulation Enhances Re-Epithelialization via Keratinocyte Activation in Full-Thickness Skin Wounds.","authors":"Joo Hyun Kim, Delgerzul Baatar, Myung Jin Ban, Ji Won Son, Jihye Choi, Chan Hee Gil, Min-Kyu Kim, Sung Sik Hur, Jung Eun Kim, Yongsung Hwang","doi":"10.3390/cells14181415","DOIUrl":"10.3390/cells14181415","url":null,"abstract":"<p><p>Chronic wound healing is a complex and tightly regulated process requiring coordinated epithelial and stromal regeneration. Photobiomodulation (PBM) using low-level red light-emitting diode (LED) therapy has emerged as a non-invasive approach to enhancing skin repair. In this study, we evaluated the therapeutic efficacy of a pulsed, multi-wavelength LED system on full-thickness excisional wound healing in a normal murine model. Daily LED treatment significantly accelerated wound closure, promoted re-epithelialization, and improved dermal architecture. Histological and immunohistochemical analyses revealed enhanced epidermal stratification, reduced inflammation, and improved collagen organization. Molecular profiling demonstrated increased expression of proliferation marker Ki67, keratins CK14 and CK17, and extracellular matrix-related genes including MMPs, Col1a1, and Col3a1. In vitro assays using HaCaT keratinocytes showed accelerated scratch wound closure and cytoskeletal remodeling following PBM exposure. These findings suggest that pulsed PBM promotes coordinated epithelial regeneration and matrix remodeling, highlighting its potential as a tunable and effective therapeutic modality for accelerating cutaneous wound healing under physiological conditions.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468576/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148163","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":"TIMP-1 Modulation Correlates with KRAS Dependency and EMT Induction in NSCLC.","authors":"Ilamathi M-Thirusenthilarasan, Pankaj Ahluwalia, Nithyananda Thorenoor, Sampa Ghoshal-Gupta, Byung Rho Lee, Bilal Siddiqui, Ravindra Kolhe, Amyn M Rojiani, Mumtaz V Rojiani","doi":"10.3390/cells14181413","DOIUrl":"10.3390/cells14181413","url":null,"abstract":"<p><p>Kirsten rat sarcoma viral oncogene homolog (KRAS) is one of the most frequently mutated genes in human cancer, including non-small cell lung carcinoma (NSCLC). Sustained expression of KRAS is required for survival in KRAS-dependent tumors. KRAS tumors can become independent upon bypassing this addiction. Tissue inhibitor of metalloproteinase-1 (TIMP-1) exhibits a range of novel functions in addition to its initially recognized activity as a physiological inhibitor of matrix metalloproteinases (MMPs). It has repeatedly been associated with cancer progression and poor prognosis in multiple cancers. This study investigates the relationship between TIMP-1 modulation and KRAS dependency in NSCLC. We found an inverse expression of KRAS and TIMP-1 in NSCLC lines. Modulating TIMP-1 levels altered KRAS expression and affected KRAS-dependency features. Overexpression of TIMP-1 decreases the KRAS levels in dependent cells and knocking-down TIMP-1 increases KRAS levels in independent cells with concomitant change in RAS-GTP levels. TIMP-1 modulation influenced apoptosis upon KRAS ablation, with TIMP-1 overexpression decreasing apoptosis in dependent cells and TIMP-1 knockdown increasing it in independent cells. Bioinformatic analysis depicted variant-specific perturbations between KRAS and TIMP-1 expression. Furthermore, EMT marker expression was altered upon TIMP-1 modulation, suggesting the role of TIMP-1 in EMT induction in KRAS-independent cells. These findings emphasize the intricate relationship between TIMP-1 and KRAS in NSCLC, shedding light on potential mechanisms underlying tumor behavior and response to therapy.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147840","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":"Transcriptomic Alteration in FUS-ALS Points Towards Apoptosis-Rather than Ferroptosis-Related Cell Death Pathway.","authors":"Banaja P Dash, Andreas Hermann","doi":"10.3390/cells14181417","DOIUrl":"10.3390/cells14181417","url":null,"abstract":"<p><p>Amyotrophic lateral sclerosis (ALS) is a fatal type of neurodegenerative disease marked by progressive and selective degeneration of motor neurons (MNs) present in the spinal cord, brain stem and motor cortex. However, the intricate molecular mechanisms underlying primary cell death pathways, including ferroptosis-related genes (FRGs) mediating MN dysfunction in ALS, remain elusive. Ferroptosis, a novel type of iron-dependent cell death with the accumulation of lipid peroxidation products, stands distinct from apoptotic-related stress and other cell death mechanisms. Although growing advances have highlighted the role of iron deposition, apoptosis and alteration of antioxidant systems in ALS pathogenesis, there is little data at the systems biology level. Therefore, we performed a comprehensive bioinformatic analysis of bulk RNA-sequencing (RNA-seq) data by systematically comparing the gene expression profiles from iPSC-derived MNs of ALS patients and healthy controls using our datasets as well as from the GEO database to reveal the role of ferroptosis-related gene alterations in ALS, especially in selective MN vulnerability of <i>FUSED IN SARCOMA</i> (<i>FUS</i>) mutations. In this study, we first identified differentially expressed genes (DEGs) between <i>FUS</i> mutant and healthy controls. Subsequently, the crossover genes between DEGs and FRGs were selected as differentially expressed ferroptosis-related genes (DEFRGs). Functional enrichment and protein-protein interaction (PPI) analysis of DEFRGs identified that DNA damage, stress response and extra cellular matrix (ECM) were the most significantly dysregulated functions/pathways in <i>FUS</i>-ALS causing mutations compared to healthy controls. While GSEA analysis showed enrichment of genes associated with apoptosis, the degree of ferroptosis and iron ion homeostasis/response to iron of <i>FUS</i> MNs was lower. Altogether, our findings may contribute to a better understanding of the relevant role of cell death pathways underlying selective vulnerability of MNs to neurodegeneration in <i>FUS</i>-ALS pathophysiology.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12468769/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147925","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":"RETRACTED: Zuccarini et al. Multipotent Stromal Cells from Subcutaneous Adipose Tissue of Normal Weight and Obese Subjects: Modulation of Their Adipogenic Differentiation by Adenosine A₁ Receptor Ligands. <i>Cells</i> 2021, <i>10</i>, 3560.","authors":"Mariachiara Zuccarini, Catia Lambertucci, Marzia Carluccio, Patricia Giuliani, Maurizio Ronci, Andrea Spinaci, Rosaria Volpini, Renata Ciccarelli, Patrizia Di Iorio","doi":"10.3390/cells14181414","DOIUrl":"10.3390/cells14181414","url":null,"abstract":"<p><p>The journal retracts the article titled \"Multipotent Stromal Cells from Subcutaneous Adipose Tissue of Normal Weight and Obese Subjects: Modulation of Their Adipogenic Differentiation by Adenosine A₁ Receptor Ligands\" [...].</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 18","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12422597/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032845","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}