Human Oncostatin M (OSM) is a multifunctional cytokine belonging to the IL-6 cytokine family, which also includes IL-6, IL-11, leukemia inhibitory factor (LIF), cardiotrophin-1 (CT-1), ciliary neurotrophic factor (CNTF), cardiotrophin-like cytokine factor 1 (CLCF1), and IL-27. OSM signals through receptor complexes containing the shared gp130 (IL6ST) subunit together with either the oncostatin M receptor (OSMR) or leukemia inhibitory factor receptor (LIFR), leading to activation of intracellular signaling pathways such as JAK/STAT (particularly STAT3), MAPK, and PI3K/AKT. Human OSM is produced mainly by activated T lymphocytes, monocytes/macrophages, neutrophils, and dendritic cells and plays important roles in regulating inflammation, hematopoiesis, immune responses, and tissue remodeling. OSM influences the behavior of endothelial cells, fibroblasts, epithelial cells, and hepatocytes, promoting cytokine production, acute-phase responses, and extracellular matrix remodeling. Dysregulated OSM signaling has been implicated in several chronic inflammatory and autoimmune diseases, including rheumatoid arthritis, inflammatory bowel disease, psoriasis, and pulmonary or liver fibrosis, where it contributes to persistent inflammatory signaling and tissue damage. OSM is also involved in cancer biology, influencing tumor cell proliferation, angiogenesis, and tumor microenvironment remodeling in cancers such as breast, colorectal, and pancreatic cancer. Because of its central role in inflammation and tissue remodeling, human OSM is widely studied as both a biomarker and therapeutic target in inflammatory disease, fibrosis, and oncology.