Key result
Oncostatin M is highly expressed in chronic inflammatory conditions and plays a context-dependent role in various stages of the fibrotic process, including inflammation and fibroblast activation.
This review highlights the role of Oncostatin M in the fibrotic process, suggesting it as a potential therapeutic target for chronic inflammatory conditions characterized by fibrosis.
Does not support clinical targeting of Oncostatin M; leaves open prospective validation in fibrotic diseases.
Oncostain M, a member of the IL-6 family of cytokines, is produced by immune cells in response to infections and tissue injury. OSM has a broad, often context-dependent effect on various cellular processes including differentiation, hematopoiesis, cell proliferation, and cell survival. OSM signaling is initiated by binding to type I (LIFRβ/gp130) or type II (OSMRβ/gp130) receptor complexes and involves activation of Janus kinase/signal transducer and activator of transcription, mitogen-activated protein kinase, and phosphatidylinositol-3-kinase. High levels of OSM have been detected in many chronic inflammatory conditions characterized by fibrosis, giving a rationale to target OSM for the treatment of these diseases. Here we discuss the current knowledge on the role of OSM in various stages of the fibrotic process including inflammation, vascular dysfunction, and activation of fibroblasts.
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Stawski et al. (2018) conducted a review in Fibrosis. Oncostatin M was evaluated. Oncostatin M is highly expressed in chronic inflammatory conditions and plays a context-dependent role in various stages of the fibrotic process, including inflammation and fibroblast activation.
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