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.

increasing amount of attention because of its involvement in various diseases, such as idiopathic pulmonary fibrosis thus far, at least three antagonists have entered phase Ⅱ clinical trials for idiopathic pulmonary fibrosis entered phase Ⅰ clinical trials for positron emission tomography (PET) imaging of idiopathic pulmonary fibrosis

We also review the hierarchy of signaling events driving the fibrotic response and the communications explore what such connections between the cell surface and nuclear GPCR signaling might mean for cardiac fibrosis

Pharmacological targeting of cGAS/STING-YAP axis suppresses pathological angiogenesis and ameliorates organ fibrosis "Organ fibrosis is accompanied by pathological angiogenesis. Discovering new ways to ameliorate pathological angiogenesis may bypass organ fibrosis. cells. cGAS genetic deletion promoted liver and kidney fibrosis and pathological angiogenesis, including Together, our data support that activation of cGAS/STING signaling mitigates organ fibrosis and suppresses

Cell-Type-Specific Effects of the Ovarian Cancer G-Protein Coupled Receptor (OGR1) on Inflammation and Fibrosis ; Potential Implications for Idiopathic Pulmonary Fibrosis "Idiopathic pulmonary fibrosis (IPF) is a that a combination of epithelial injury and myofibroblast differentiation drives progressive pulmonary fibrosis Given the important roles of extracellular pH in the progression of pulmonary fibrosis, we sought to Proton-sensing G-protein coupled receptors are activated by acidic environments, but their role in fibrosis

This week's highlight: Congrats to our partner GPCR Therapeutics, on their expansion into fibrosis with Antibodies Against Difficult and Conserved Protein Targets GPCR Therapeutics Expands Pipeline into Fibrosis

immune cells in a range of pro-inflammatory settings and clinical trials to treat idiopathic pulmonary fibrosis

immune cells in a range of pro‐inflammatory disorders renders it a promising target in inflammatory and fibrotic neuroinflammation (Audoy‐Remus et al., 2015), with ongoing clinical trials in idiopathic pulmonary fibrosis

Investigational LPA1 Antagonist Reduces the Rate of Lung Function Decline in Patients with Idiopathic Pulmonary Fibrosis

GPR97 deficiency ameliorates renal interstitial fibrosis in mouse hypertensive nephropathy.

Regulate the Release of Superoxide Anions GPR176 promotes fibroblast-to-myofibroblast transition in organ fibrosis

β-arrestin-2 can stimulate PP2A to dephosphorylation Smad3 (inhibition) and GSK3β (activation), thus reduces fibrosis

GPCRs in Cardiology, Endocrinology, and Taste GPR97 deficiency ameliorates renal interstitial fibrosis

Therapeutics Announces Out-Licensing Agreement with Bridge Biotherapeutics in Idiopathic Pulmonary Fibrosis

Immunology Wnt pathway inhibition with the porcupine inhibitor LGK974 decreases trabecular bone but not fibrosis in a murine model with fibrotic bone The orphan G protein-coupled receptor 141 expressed in myeloid

receptor GPR52 Endosome positioning coordinates spatially selective GPCR signaling GRK5 promoted renal fibrosis

lipopolysaccharide (LPS) and TNFα suggests that it may play a role in the development of inflammatory and fibrotic