biostudies-literatureChen SShanghai Municipal Science and Technology Commission Original Exploration ProjectTongji University Independent and Original Basic Research ProjectPostdoctoral Science Foundation of ChinaNational Postdoctoral Program for Innovative TalentClinical research plan of SHDCShanghai Municipal Key Specialty ProjectNational Natural Science Foundation of ChinaShanghai Clinical Research Center for Digestive DiseasesShuimu Tsinghua Scholar Programe2306066https://www.ebi.ac.uk/biostudies/studies/S-EPMC11040347biostudies-literatureUnknown11(16)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 amoAdvanced science (Weinheim, Baden-Wurttemberg, Germany)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.PMC11040347BX2023017421ZR1481600SHSLCZDZK0680122120220647818201008006SHDC2020CR2030B2023M741963U22A202752023SM06519MC1910200Li JLu ZJia HWang FYang BZuo SZhang SYang CZhao YLi SXia LJin MLiu CChen SWang ZfalseMyeloid-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.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 amo2024-01-01T00:00:00Z2024 Apr2026-07-15T03:07:17.893Z2025-04-06T03:14:47.264ZS-EPMC110403473835072510.1002/advs.202306066