Oncostatin M and its role in fibrosis

ABSTRACT

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.

KEYWORDS:

• ECM
• fibrosis
• inflammation
• OSM
• vascular injury

Declaration of interest

The authors report no conflicts of interest.

Additional information

Funding

This work was supported by the National Institutes of Health (NIAMS) grant RO1 AR42334-19 and the NIH T32 5T32AR007598-19.