August 2022 "Aims: The pathophysiological mechanism(s) underlying non-alcoholic fatty liver disease (NAFLD) have yet to be fully delineated and only a single drug, peroxisome proliferator-activated receptor (PPAR) α/γ agonist saroglitazar, has been approved. Here, we sought to investigate the role of Regulator of G Protein Signaling 7 (RGS7) in hyperlipidemia-dependent hepatic dysfunction. " Read more at the source #DrGPCR #GPCR #IndustryNews

sclerosis (SSc) is a systemic autoimmune disease with the key features of inflammation, vasculopathy and fibrosis

Hepatic fibrosis is a critical prognostic factor in NAFLD/NASH. Therefore, a better understanding of the pathophysiology of hepatic fibrosis and the development of related However, our knowledge of how GPCRs regulate liver metabolism and fibrosis in the different cell types understanding of the role of GPCRs in hepatic stellate cells (HSCs), the primary cells that regulate liver fibrosis , may lead to the development of drugs that can improve hepatic fibrosis in NAFLD/NASH.

< GPCRs in Oncology and Immunology GPR176 promotes fibroblast-to-myofibroblast transition in organ fibrosis progression Published date July 22, 2024 Abstract "Fibrosis is characterized by excessive deposition In gene expression analysis of mouse lungs with induced fibrosis, eight GPCRs were identified, showing a >2-fold increase in mRNA expression after fibrosis induction. by fibrosis, including the kidney, liver, and heart, suggesting its role in fibrosis across various

Immunology Wnt pathway inhibition with the porcupine inhibitor LGK974 decreases trabecular bone but not fibrosis in a murine model with fibrotic bone Published date May 1, 2024 Abstract "G protein-coupled receptors Fibrous dysplasia (FD) of the bone is characterized by fibrotic, expansile bone lesions caused by activating Bone fibrosis remained evident after treatment. These results provide new insights into the role of Wnt and Gs-signaling in fibrosis and bone formation

at NIAID/NIH, where I characterized the role of RGS4 and RGS5 in airway hyperresponsiveness and lung fibrosis