{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chen S"],"funding":["Shanghai Municipal Science and Technology Commission Original Exploration Project","Tongji University Independent and Original Basic Research Project","Postdoctoral Science Foundation of China","National Postdoctoral Program for Innovative Talent","Clinical research plan of SHDC","Shanghai Municipal Key Specialty Project","National Natural Science Foundation of China","Shanghai Clinical Research Center for Digestive Diseases","Shuimu Tsinghua Scholar Program"],"pagination":["e2306066"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11040347"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(16)"],"pubmed_abstract":["Acetaminophen overdose is a leading cause of acute liver failure (ALF). Despite the pivotal role of the inflammatory microenvironment in the progression of advanced acetaminophen-induced liver injury (AILI), a comprehensive understanding of the underlying cellular interactions and molecular mechanisms remains elusive. Mas is a G protein-coupled receptor highly expressed by myeloid cells; however, its role in the AILI microenvironment remains to be elucidated. A multidimensional approach, including single-cell RNA sequencing, spatial transcriptomics, and hour-long intravital imaging, is employed to characterize the microenvironment in Mas1 deficient mice at the systemic and cell-specific levels. The characteristic landscape of mouse AILI models involves reciprocal cellular communication amo"],"journal":["Advanced science (Weinheim, Baden-Wurttemberg, Germany)"],"pubmed_title":["Myeloid-Mas Signaling Modulates Pathogenic Crosstalk among MYC<sup>+</sup>CD63<sup>+</sup> Endothelial Cells, MMP12<sup>+</sup> Macrophages, and Monocytes in Acetaminophen-Induced Liver Injury."],"pmcid":["PMC11040347"],"funding_grant_id":["BX20230174","21ZR1481600","SHSLCZDZK06801","22120220647","818201008006","SHDC2020CR2030B","2023M741963","U22A20275","2023SM065","19MC1910200"],"pubmed_authors":["Li J","Lu Z","Jia H","Wang F","Yang B","Zuo S","Zhang S","Yang C","Zhao Y","Li S","Xia L","Jin M","Liu C","Chen S","Wang Z"],"additional_accession":[]},"is_claimable":false,"name":"Myeloid-Mas Signaling Modulates Pathogenic Crosstalk among MYC<sup>+</sup>CD63<sup>+</sup> Endothelial Cells, MMP12<sup>+</sup> Macrophages, and Monocytes in Acetaminophen-Induced Liver Injury.","description":"Acetaminophen overdose is a leading cause of acute liver failure (ALF). Despite the pivotal role of the inflammatory microenvironment in the progression of advanced acetaminophen-induced liver injury (AILI), a comprehensive understanding of the underlying cellular interactions and molecular mechanisms remains elusive. Mas is a G protein-coupled receptor highly expressed by myeloid cells; however, its role in the AILI microenvironment remains to be elucidated. A multidimensional approach, including single-cell RNA sequencing, spatial transcriptomics, and hour-long intravital imaging, is employed to characterize the microenvironment in Mas1 deficient mice at the systemic and cell-specific levels. The characteristic landscape of mouse AILI models involves reciprocal cellular communication amo","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Apr","modification":"2026-07-15T03:07:17.893Z","creation":"2025-04-06T03:14:47.264Z"},"accession":"S-EPMC11040347","cross_references":{"pubmed":["38350725"],"doi":["10.1002/advs.202306066"]}}