tbuckley/cabot-search huggingface dataset:
Tissue-engineered mesenchymal stem cell constructs alleviate tendinopathy by suppressing vascularization
Authors: Dijun Li, Jingwei Jiu, Haifeng Liu, Xiaojun Yan, Xiaoke Li, Lei Yan, Jing Zhang, Zijuan Fan, Songyan Li, Guangyuan Du, Jiao Jiao Li, Yanan Du, Wei Liu, Bin Wang
Journal: Bioactive Materials (2024)

Tendinopathy leads to low-grade tissue inflammation and chronic damage, which progresses due to pathological imbalance in angiogenesis. Reducing early pathological vascularization may be a new approach in helping to regenerate tendon tissue. Conventional stem cell therapy and tissue engineering scaffolds have not been highly effective at treating tendinopathy. In this study, tissue engineered stem cells (TSCs) generated using human umbilical cord mesenchymal stem cells (hUC-MSCs) were combined with microcarrier scaffolds to limit excessive vascularization in tendinopathy. By preventing VEGF receptor activation through their paracrine function, TSCs reduced in vitro angiogenesis and the proliferation of vascular endothelial cells. TSCs also decreased the inflammatory expression of tenocytes while promoting their anabolic and tenogenic characteristics. Furthermore, local injection of TSCs into rats with collagenase-induced tendinopathy substantially reduced early inflammation and vascularization. Mechanistically, transcriptome sequencing revealed that TSCs could reduce the progression of pathological angiogenesis in tendon tissue, attributed to Rap1-mediated vascular inhibition. TSCs may serve as a novel and practical approach for suppressing tendon vascularization, and provide a promising therapeutic agent for early-stage clinical tendinopathy.
Cu(II)-baicalein enhance paracrine effect and regenerative function of stem cells in patients with diabetes
Authors: Kaijing Liu, Ruihao Li, Shusen Wang, Xue Fu, Ni Zhu, Xiaoyu Liang, Huiyang Li, Xiaoli Wang, Le Wang, Yongjun Li, Jianwu Dai, Jing Yang
Journal: Bioactive Materials (2024)

The development of engineered or modified autologous stem cells is an effective strategy to improve the efficacy of stem cell therapy. In this study, the stemness and functionality of adipose stem cells derived from type 1 diabetic donors (T1DM-ASC) were enhanced by treatment with Cu(II)-baicalein microflowers (Cu-MON). After treatment with Cu-MON, T1DM-ASC showed enhanced expression of the genes involved in the cytokine-cytokine receptor interaction pathway and increased cytokine secretion. Among the top 13 differentially expressed genes between T1DM-ASC and Cu-MON-treated T1DM-ASC (CMTA), some genes were also expressed in HUVEC, Myoblast, Myofibroblast, and Vascular Smooth Muscle cells, inferring the common role of these cell types. In vivo experiments showed that CMTA had the same therapeutic effect as adipose-derived stem cells from non-diabetic donors (ND-ASC) at a 15% cell dose, greatly reducing the treatment cost. Taken together, these findings suggest that Cu-MON promoted angiogenesis by promoting the stemness and functionality of T1DM-ASC and influencing multiple overall repair processes, including paracrine effects.
Gut microbiota DPP4-like enzymes are increased in type-2 diabetes and contribute to incretin inactivation
Authors: Marta Olivares, Paula Hernández-Calderón, Sonia Cárdenas-Brito, Rebeca Liébana-García, Yolanda Sanz, Alfonso Benítez-Páez
Journal: Genome biology (2024)

Abstract Background The gut microbiota controls broad aspects of human metabolism and feeding behavior, but the basis for this control remains largely unclear. Given the key role of human dipeptidyl peptidase 4 (DPP4) in host metabolism, we investigate whether microbiota DPP4-like counterparts perform the same function. Results We identify novel functional homologs of human DPP4 in several bacterial species inhabiting the human gut, and specific associations between Parabacteroides and Porphyromonas DPP4-like genes and type 2 diabetes (T2D). We also find that the DPP4-like enzyme from the gut symbiont Parabacteroides merdae mimics the proteolytic activity of the human enzyme on peptide YY, neuropeptide Y, gastric inhibitory polypeptide (GIP), and glucagon-like peptide 1 (GLP-1) hormones in vitro. Importantly, administration of E. coli overexpressing the P. merdae DPP4-like enzyme to lipopolysaccharide-treated mice with impaired gut barrier function reduces active GIP and GLP-1 levels, which is attributed to increased DPP4 activity in the portal circulation and the cecal content. Finally, we observe that linagliptin, saxagliptin, sitagliptin, and vildagliptin, antidiabetic drugs with DPP4 inhibitory activity, differentially inhibit the activity of the DPP4-like enzyme from P. merdae . Conclusions Our findings confirm that proteolytic enzymes produced by the gut microbiota are likely to contribute to the glucose metabolic dysfunction that underlies T2D by inactivating incretins, which might inspire the development of improved antidiabetic therapies.
Central nervous system-associated macrophages modulate the immune response following stroke in aged mice
Authors: Damien Levard, Célia Seillier, Mathys Bellemain-Sagnard, Antoine Philippe Fournier, Eloïse Lemarchand, Chantal Dembech, Gaëtan Riou, Karina McDade, Colin Smith, Conor McQuaid, Axel Montagne, Lukas Amann, Marco Prinz, Denis Vivien, Marina Rubio
Journal: Nature Neuroscience (2024)
Sex-dependent APOE4 neutrophil–microglia interactions drive cognitive impairment in Alzheimer’s disease
Authors: Neta Rosenzweig, Kilian L. Kleemann, Thomas Rust, Madison Carpenter, Madeline Grucci, Michael Aronchik, Nieske Brouwer, Isabel Valenbreder, Joya Cooper-Hohn, Malvika Iyer, Rajesh K. Krishnan, Kisha N. Sivanathan, Wesley Brandão, Taha Yahya, Ana Durao, Zhuoran Yin, Jean Paul Chadarevian, Michael J. Properzi, Roni Nowarski, Hayk Davtyan, Howard L. Weiner, Mathew Blurton-Jones, Hyun-Sik Yang, Bart J. L. Eggen, Reisa A. Sperling, Oleg Butovsky
Journal: Nature Medicine (2024)
SETDB1 regulates short interspersed nuclear elements and chromatin loop organization in mouse neural precursor cells
Authors: Daijing Sun, Yueyan Zhu, Wenzhu Peng, Shenghui Zheng, Jie Weng, Shulong Dong, Jiaqi Li, Qi Chen, Chuanhui Ge, Liyong Liao, Yuhao Dong, Yun Liu, Weida Meng, Yan Jiang
Journal: Genome biology (2024)

Abstract Background Transposable elements play a critical role in maintaining genome architecture during neurodevelopment. Short Interspersed Nuclear Elements (SINEs), a major subtype of transposable elements, are known to harbor binding sites for the CCCTC-binding factor (CTCF) and pivotal in orchestrating chromatin organization. However, the regulatory mechanisms controlling the activity of SINEs in the developing brain remains elusive. Results In our study, we conduct a comprehensive genome-wide epigenetic analysis in mouse neural precursor cells using ATAC-seq, ChIP-seq, whole genome bisulfite sequencing, in situ Hi-C, and RNA-seq. Our findings reveal that the SET domain bifurcated histone lysine methyltransferase 1 (SETDB1)-mediated H3K9me3, in conjunction with DNA methylation, restricts chromatin accessibility on a selective subset of SINEs in neural precursor cells. Mechanistically, loss of Setdb1 increases CTCF access to these SINE elements and contributes to chromatin loop reorganization. Moreover, de novo loop formation contributes to differential gene expression, including the dysregulation of genes enriched in mitotic pathways. This leads to the disruptions of cell proliferation in the embryonic brain after genetic ablation of Setdb1 both in vitro and in vivo . Conclusions In summary, our study sheds light on the epigenetic regulation of SINEs in mouse neural precursor cells, suggesting their role in maintaining chromatin organization and cell proliferation during neurodevelopment.
A deep-learning framework to predict cancer treatment response from histopathology images through imputed transcriptomics
Authors: Danh-Tai Hoang, Gal Dinstag, Eldad D. Shulman, Leandro C. Hermida, Doreen S. Ben-Zvi, Efrat Elis, Katherine Caley, Stephen-John Sammut, Sanju Sinha, Neelam Sinha, Christopher H. Dampier, Chani Stossel, Tejas Patil, Arun Rajan, Wiem Lassoued, Julius Strauss, Shania Bailey, Clint Allen, Jason Redman, Tuvik Beker, Peng Jiang, Talia Golan, Scott Wilkinson, Adam G. Sowalsky, Sharon R. Pine, Carlos Caldas, James L. Gulley, Kenneth Aldape, Ranit Aharonov, Eric A. Stone, Eytan Ruppin
Journal: Nature Cancer (2024)
A unified metric of human immune health
Authors: Rachel Sparks, Nicholas Rachmaninoff, William W. Lau, Dylan C. Hirsch, Neha Bansal, Andrew J. Martins, Jinguo Chen, Candace C. Liu, Foo Cheung, Laura E. Failla, Angelique Biancotto, Giovanna Fantoni, Brian A. Sellers, Daniel G. Chawla, Katherine N. Howe, Darius Mostaghimi, Rohit Farmer, Yuri Kotliarov, Katherine R. Calvo, Cindy Palmer, Janine Daub, Ladan Foruraghi, Samantha Kreuzburg, Jennifer D. Treat, Amanda K. Urban, Anne Jones, Tina Romeo, Natalie T. Deuitch, Natalia Sampaio Moura, Barbara Weinstein, Susan Moir, Luigi Ferrucci, Karyl S. Barron, Ivona Aksentijevich, Steven H. Kleinstein, Danielle M. Townsley, Neal S. Young, Pamela A. Frischmeyer-Guerrerio, Gulbu Uzel, Gineth Paola Pinto-Patarroyo, Cornelia D. Cudrici, Patrycja Hoffmann, Deborah L. Stone, Amanda K. Ombrello, Alexandra F. Freeman, Christa S. Zerbe, Daniel L. Kastner, Steven M. Holland, John S. Tsang
Journal: Nature Medicine (2024)
Disruption of intestinal oxygen balance in acute colitis alters the gut microbiome
Authors: Wenjing Zong, Elliot S. Friedman, Srinivasa Rao Allu, Jenni Firrman, Vincent Tu, Scott G. Daniel, Kyle Bittinger, LinShu Liu, Sergei A. Vinogradov, Gary D. Wu
Journal: Gut Microbes (2024)

The juxtaposition of well-oxygenated intestinal colonic tissue with an anerobic luminal environment supports a fundamentally important relationship that is altered in the setting of intestinal injury, a process likely to be relevant to diseases such as inflammatory bowel disease. Herein, using two-color phosphorometry to non-invasively quantify both intestinal tissue and luminal oxygenation in real time, we show that intestinal injury induced by DSS colitis reduces intestinal tissue oxygenation in a spatially defined manner and increases the flux of oxygen from the tissue into the gut lumen. By characterizing the composition of the microbiome in both DSS colitis-affected gut and in a bioreactor containing a stable human fecal community exposed to microaerobic conditions, we provide evidence that the increased flux of oxygen into the gut lumen augments glycan degrading bacterial taxa rich in glycoside hydrolases which are known to inhabit gut mucosal surface. Continued disruption of the intestinal mucus barrier through such a mechanism may play a role in the perpetuation of the intestinal inflammatory process.
mTORC1 Signaling in Brain Endothelial Progenitors Contributes to CCM Pathogenesis
Authors: Wang Min, Lingfeng Qin, Haifeng Zhang, Francesc López-Giráldez, Ning Jiang, Yeaji Kim, Varsha K. Mohan, Minhong Su, Katie N. Murray, Jaime Grutzendler, Jenny Huanjiao Zhou
Journal: Circulation Research (2024)

BACKGROUND: Cerebral vascular malformations (CCMs) are primarily found within the brain, where they result in increased risk for stroke, seizures, and focal neurological deficits. The unique feature of the brain vasculature is the blood-brain barrier formed by the brain neurovascular unit. Recent studies suggest that loss of CCM genes causes disruptions of blood-brain barrier integrity as the inciting events for CCM development. CCM lesions are proposed to be initially derived from a single clonal expansion of a subset of angiogenic venous capillary endothelial cells (ECs) and respective resident endothelial progenitor cells (EPCs). However, the critical signaling events in the subclass of brain ECs/EPCs for CCM lesion initiation and progression are unclear. METHODS: Brain EC-specific CCM3-deficient ( Pdcd10 BECKO ) mice were generated by crossing Pdcd10 fl/fl mice with Mfsd2a -CreER T2 mice. Single-cell RNA-sequencing analyses were performed by the chromium single-cell platform (10× genomics). Cell clusters were annotated into EC subtypes based on visual inspection and GO analyses. Cerebral vessels were visualized by 2-photon in vivo imaging and tissue immunofluorescence analyses. Regulation of mTOR (mechanistic target of rapamycin) signaling by CCM3 and Cav1 (caveolin-1) was performed by cell biology and biochemical approaches. RESULTS: Single-cell RNA-sequencing analyses from P10 Pdcd1 0 BECKO mice harboring visible CCM lesions identified upregulated CCM lesion signature and mitotic EC clusters but decreased blood-brain barrier–associated EC clusters. However, a unique EPC cluster with high expression levels of stem cell markers enriched with mTOR signaling was identified from early stages of the P6 Pdcd1 0 BECKO brain. Indeed, mTOR signaling was upregulated in both mouse and human CCM lesions. Genetic deficiency of Raptor (regulatory-associated protein of mTOR), but not of Rictor (rapamycin-insensitive companion of mTOR), prevented CCM lesion formation in the Pdcd10 BECKO model. Importantly, the mTORC1 (mTOR complex 1) pharmacological inhibitor rapamycin suppressed EPC proliferation and ameliorated CCM pathogenesis in Pdcd10 BECKO mice. Mechanistic studies suggested that Cav1/caveolae increased in CCM3-depleted EPC-mediated intracellular trafficking and complex formation of the mTORC1 signaling proteins. CONCLUSIONS: CCM3 is critical for maintaining blood-brain barrier integrity and CCM3 loss–induced mTORC1 signaling in brain EPCs initiates and facilitates CCM pathogenesis.
Transcriptomic Differences in Medullary Thyroid Carcinoma According to Grade
Authors: Ignacio Ruz-Caracuel, Tamara Caniego-Casas, Teresa Alonso-Gordoa, Irene Carretero-Barrio, Carmen Ariño-Palao, Almudena Santón, Marta Rosas, Héctor Pian, Javier Molina-Cerrillo, Patricia Luengo, José Palacios
Journal: Endocrine Pathology (2024)

Abstract Medullary thyroid carcinoma (MTC) is a rare cancer derived from neuroendocrine C-cells of the thyroid. In contrast to other neuroendocrine tumors, a histological grading system was lacking until recently. A novel two-tier grading system based on the presence of high proliferation or necrosis is associated with prognosis. Transcriptomic analysis was conducted on 21 MTCs, including 9 high-grade tumors, with known mutational status, using the NanoString Tumor Signaling 360 Panel. This analysis, covering 760 genes, revealed upregulation of the genes EGLN3 , EXO1 , UBE2T , UBE2C , FOXM1 , CENPA , DLL3 , CCNA2 , SOX2 , KIF23 , and CDCA5 in high-grade MTCs. Major pathways differentially expressed between high-grade and low-grade MTCs were DNA damage repair, p53 signaling, cell cycle, apoptosis, and Myc signaling. Validation through qRT-PCR in 30 MTCs demonstrated upregulation of ASCL1 , DLL3 , and SOX2 in high-grade MTCs, a gene signature akin to small-cell lung carcinoma, molecular subgroup A. Subsequently, DLL3 expression was validated by immunohistochemistry. MTCs with DLL3 overexpression (defined as ≥ 50% of positive tumor cells) were associated with significantly lower disease-free survival ( p = 0.041) and overall survival ( p = 0.01). Moreover, MTCs with desmoplasia had a significantly increased expression of DLL3. Our data supports the idea that DLL3 should be further explored as a predictor of aggressive disease and poor outcomes in MTC.
Cardiomyocyte PANX1 Controls Glycolysis and Neutrophil Recruitment in Hypertrophy
Authors: Caitlin M. Pavelec, Alexander P. Young, Hannah L. Luviano, Emily E. Orrell, Anna Szagdaj, Nabin Poudel, Abigail G. Wolpe, Samantha H. Thomas, Scott Yeudall, Clint M. Upchurch, Mark D. Okusa, Brant E. Isakson, Matthew J. Wolf, Norbert Leitinger
Journal: Circulation Research (2024)

PANX1 (pannexin 1), a ubiquitously expressed ATP release membrane channel, has been shown to play a role in inflammation, blood pressure regulation, and myocardial infarction. However, the possible role of PANX1 in cardiomyocytes in the progression of heart failure has not yet been investigated.
Correction: Profiling chromatin accessibility in pediatric acute lymphoblastic leukemia identifies subtype-specific chromatin landscapes and gene regulatory networks
Authors: Jonathan D. Diedrich, Qian Dong, Daniel C. Ferguson, Brennan P. Bergeron, Robert J. Autry, Maoxiang Qian, Wenjian Yang, Colton Smith, James B. Papizan, Jon P. Connelly, Kohei Hagiwara, Kristine R. Crews, Shondra M. Pruett-Miller, Ching-Hon Pui, Jun J. Yang, Mary V. Relling, William E. Evans, Daniel Savic
Journal: Leukemia (2024)
Contrast-enhanced mammography versus conventional imaging in women recalled from breast cancer screening (RACER trial): a multicentre, open-label, randomised controlled clinical trial
Authors: Lidewij M F H Neeter, Patricia J Nelemans, H P J Raat, Caroline Frotscher, Katya M Duvivier, Brigitte A B Essers, Marjolein L Smidt, Joachim E Wildberger, Marc B I Lobbes
Journal: The Lancet Regional Health - Europe (2024)

Women recalled from breast cancer screening receive post-screening work-up in the hospital with conventional breast imaging. The RACER trial aimed to study whether contrast-enhanced mammography (CEM) as primary imaging instead of conventional imaging resulted in more accurate and efficient diagnostic work-up in recalled women.
ROS-responsive and triple-synergistic mitochondria-targeted polymer micelles for efficient induction of ICD in tumor therapeutics
Authors: Xiaoxiao Hu, Mo Zhang, Cuilu Quan, Saisai Ren, Wei Chen, Jing Wang
Journal: Bioactive Materials (2024)

Immunogenic cell death (ICD) represents a modality of apoptosis distinguished by the emanation of an array of damage-related molecular signals. This mechanism introduces a novel concept in the field of contemporary tumor immunotherapy. The inception of reactive oxygen species (ROS) within tumor cells stands as the essential prerequisite and foundation for ICD induction. The formulation of highly efficacious photodynamic therapy (PDT) nanomedicines for the successful induction of ICD is an area of significant scientific inquiry. In this work, we devised a ROS-responsive and triple-synergistic mitochondria-targeted polymer micelle (CAT/CPT-TPP/PEG-Ce6, CTC) that operates with multistage amplification of ROS to achieve the potent induction of ICD. Utilizing an "all-in-one" strategy, we direct both the PDT and chemotherapeutic units to the mitochondria. Concurrently, a multistage cyclical amplification that caused by triple synergy strategy stimulates continuous, stable, and adequate ROS generation (domino effect) within the mitochondria of cells. Conclusively, influenced by ROS, tumor cell-induced ICD is effectively activated, remodeling immunogenicity, and enhancing the therapeutic impact of PDT when synergized with chemotherapy. Empirical evidence from in vitro study substantiates that CTC micelles can efficiently provoke ICD, catalyzing CRT translocation, the liberation of HMGB1 and ATP. Furthermore, animal trials corroborate that polymer micelles, following tail vein injection, can induce ICD, accumulate effectively within tumor tissues, and markedly inhibit tumor growth subsequent to laser irradiation. Finally, transcriptome analysis was carried out to evaluate the changes in tumor genome induced by CTC micelles. This work demonstrates a novel strategy to improve combination immunotherapy using nanotechnology.
<scp>EBV</scp>‐positive diffuse large B‐cell lymphoma, not otherwise specified: 2024 update on the diagnosis, risk‐stratification, and management
Authors: Luis Malpica, Mario L. Marques‐Piubelli, Brady E. Beltran, Julio C. Chavez, Roberto N. Miranda, Jorge J. Castillo
Journal: American Journal of Hematology (2024)

Abstract Disease overview Epstein Barr virus‐positive (EBV+) diffuse large B‐cell lymphoma (DLBCL), not otherwise specified (NOS) is an aggressive B‐cell lymphoma associated with EBV infection included in the WHO classification of lymphoid neoplasms since 2016. Although historically associated to poor prognosis, outcomes seem to have improved in the era of chemoimmunotherapy. Diagnosis The diagnosis is established through meticulous pathological evaluation. Detection of EBV‐encoded RNA (EBER) is the standard diagnostic method. The ICC 2022 specifies EBV+ DLBCL, NOS as occurring when &gt;80% of malignant cells express EBER, whereas the WHO‐HAEM5 emphasizes that the majority of tumor cells should be EBER positive without setting a defined threshold. The differential diagnosis includes plasmablastic lymphoma, DLBCL associated with chronic inflammation, primary effusion lymphoma, among others. Risk‐stratification The International Prognostic Index (IPI) and the Oyama score can be used for risk‐stratification. The Oyama score includes age &gt;70 years and presence of B symptoms. The expression of CD30 and PD‐1/PD‐L1 are emerging as potential adverse but targetable biomarkers. Management Patients with EBV+ DLBCL, NOS, should be staged and managed following similar guidelines than patients with EBV‐negative DLBCL. EBV+ DLBCL, NOS, however, might have a worse prognosis than EBV‐negative DLBCL in the era of chemoimmunotherapy. Therefore, inclusion of patients in clinical trials when available is recommended. There is an opportunity to study and develop targeted therapy in the management of patients with EBV+ DLBCL, NOS.
ESMO Clinical Practice Guideline interim update on new targeted therapies in the first-line and at relapse of chronic lymphocytic leukaemia
Authors: B. Eichhorst, P. Ghia, C.U. Niemann, A.P. Kater, M. Gregor, M. Hallek, M. Jerkeman, C. Buske
Journal: Annals of Oncology (2024)
Dynamic Endocannabinoid-mediated Neuromodulation of Retinal Circadian Circuitry
Authors: Deepak Kumar, Bareera Khan, Yagmur Okcay, Çağıl Önal Sis, Aya Abdallah, Fiona Murray, Ashish Sharma, Maiko Uemura, Rajeev Taliyan, Thomas Heinbockel, Shafiqur Rahman, Rohit Goyal
Journal: Ageing Research Reviews (2024)
A distinct subset of urothelial cells with enhanced EMT features promotes chemotherapy resistance and cancer recurrence by increasing COL4A1-ITGB1 mediated angiogenesis
Authors: Jinan Guo, Xiaoshi Ma, Dongcheng Liu, Fei Wang, Jinquan Xia, Bin Zhang, Pan Zhao, Fuhua Zhong, Lipeng Chen, Qiaoyun Long, Lu Jiang, Siyu Zhang, Naikai Liao, Jigang Wang, Weiqing Wu, Jichao Sun, Mou Huang, Zhiqiang Cheng, Guixiao Huang, Chang Zou
Journal: Drug Resistance Updates (2024)

Drug resistance and tumor recurrence remain clinical challenges in the treatment of urothelial carcinoma (UC). However, the underlying mechanism is not fully understood. Here, we performed single-cell RNA sequencing and identified a subset of urothelial cells with epithelial-mesenchymal transition (EMT) features (EMT-UC), which is significantly correlated with chemotherapy resistance and cancer recurrence. To validate the clinical significance of EMT-UC, we constructed EMT-UC like cells by introducing overexpression of two markers, Zinc Finger E-Box Binding Homeobox 1 (ZEB1) and Desmin (DES), and examined their histological distribution characteristics and malignant phenotypes. EMT-UC like cells were mainly enriched in UC tissues from patients with adverse prognosis and exhibited significantly elevated EMT, migration and gemcitabine tolerance in vitro. However, EMT-UC was not specifically identified from tumorous tissues, certain proportion of them were also identified in adjacent normal tissues. Tumorous EMT-UC highly expressed genes involved in malignant behaviors and exhibited adverse prognosis. Additionally, tumorous EMT-UC was associated with remodeled tumor microenvironment (TME), which exhibited high angiogenic and immunosuppressive potentials compared with the normal counterparts. Furthermore, a specific interaction of COL4A1 and ITGB1 was identified to be highly enriched in tumorous EMT-UC, and in the endothelial component. Targeting the interaction of COL4A1 and ITGB1 with specific antibodies significantly suppressed tumorous angiogenesis and alleviated gemcitabine resistance of UC. Overall, our findings demonstrated that the driven force of chemotherapy resistance and recurrence of UC was EMT-UC mediated COL4A1-ITGB1 interaction, providing a potential target for future UC treatment.