Objectives: Fibroblast growth factor 23 (FGF23) became recently recognized as a heart failure (HF) marker. We found increased cardiac transcript and protein levels of this phosphatonin in patients with myocarditis, aortic stenosis, ischemic and dilated cardiomyopathy. We demonstrated previously that oncostatin M (OSM) massively induces the secretion of FGF23 by cardiomyocytes during the course of HF. Since OSM is an inflammatory cytokine we questioned whether anti-inflammatory signaling could downregulate the release of FGF23 by cardiomyocytes.

Objectives: Acute myocardial infarction (MI) results in an inflammatory response, which is considered as a key step in cardiac healing and left ventricular remodeling. This acute immune process is mainly mediated by infiltrating leukocytes to the injured myocardium. We have previously shown that the absence of the inflammatory cytokine oncostatin M (OSM) is associated with adverse remodeling after MI, but the impact of OSM signaling for cardiac inflammation remains to be elucidated.

Objectives: Previously, we found that treatment of mice with the inflammatory cytokine oncostatin M (OSM) improved cardiac function and suppressed remodeling after myocardial infarction. Since these results suggested a protective role of OSM under hypoxic conditions, we assessed whether activation of the OSM receptor (Oβ) directly affects survival of cardiomyocytes under hypoxia and alters morphology and expression of genes that are responsible for O2 handling and consumption.

Objectives: The interplay of inflammatory and anti-inflammatory cytokines attract much attention because these factors are important in organ and tissue regeneration. We have previously demonstrated that the receptors of the anti-inflammatory cytokine Interleukin-13 (Il-13) as well as the inflammatory cytokine oncostatin M (OSM) mediate highly protective activities during cardiac damage. So far Il-13 is mostly seen in the light of an anti-inflammatory mediator while little attention is paid to synergizing effects with inflammatory cytokines. We wanted to know why these cytokines with obviously two completely different features exert cardioprotective activities and whether they might act in concert.