Myeloid-Mas Signaling Modulates Pathogenic Crosstalk among MYC⁺CD63⁺ Endothelial Cells, MMP12⁺ Macrophages, and Monocytes in Acetaminophen-Induced Liver Injury.

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

SUBMITTER: Chen S 

PROVIDER: S-EPMC11040347 | biostudies-literature | 2024 Apr

REPOSITORIES: biostudies-literature