Osmr, the Oncostatin M receptor, is a crucial component in the interleukin-6 (IL-6) family cytokine signaling. It binds to Oncostatin M (OSM) through a complex with the common glycoprotein 130 (gp130) subunit, activating various downstream signaling pathways such as STAT3. This signaling is involved in numerous biological processes and is associated with chronic inflammatory, cardiovascular, and cancer-related diseases [3]. Genetic models like the Osmr conditional knockout (CKO) mouse model are valuable tools for studying Osmr function [4].

In pancreatic ductal adenocarcinoma (PDA), macrophage-secreted OSM binds to Osmr on cancer-associated fibroblasts (CAFs), reprogramming them to create a pro-tumorigenic environment and promoting tumour growth and metastasis. Tumour cells in Osm-deficient mice show reduced growth and no metastasis [1]. In cardiac hypertrophy, Osmr deficiency in mice aggravated the condition by modulating macrophages and activating the OSM/LIFR/STAT3 signalling, promoting a pro-resolving macrophage phenotype that exacerbated inflammation and impaired cardiac repair [2]. In primary localized cutaneous amyloidosis (PLCA), OSMR loss-function mutants enhanced basal keratinocyte differentiation, and the up-regulation of AHNAK due to OSMR mutations led to keratinocyte hyperproliferation and over-differentiation [5]. In glioblastoma, deletion of Osmr in glioma stem cells impaired spare respiratory capacity, increased reactive oxygen species, and sensitized the cells to ionizing radiation-induced cell death, suggesting Osmr confers radiation resistance [6].

In conclusion, Osmr plays essential roles in multiple disease-related biological processes. Studies using Osmr KO/CKO mouse models have revealed its significance in cancer, cardiac, and skin diseases, providing insights into potential therapeutic targets for these conditions.