Key result
Insulin-like growth factor-1 confers cardiac protection against ischemia via mitochondria-dependent mechanisms, though long-term exposure may enhance inflammatory responses.
This commentary highlights the role of IGF-1 in protecting myocardial tissue against ischemia via mitochondria-dependent mechanisms and its crosstalk with TNF-alpha.
Insulin-like growth factor (IGF)-1 is a well characterized growth factor that plays a role in the regulation of myocardial structure and function. Using an ex vivo murine model, Davani and coworkers, in this issue of Critical Care, demonstrate that IGF-1 confers cardiac protection against ischemia via mitochondria-dependent mechanisms. Those investigators used the ratio of mitochondrial to nuclear DNA to demonstrate that IGF-1, which prevents reduction in this ratio during reperfusion, provides cytoprotection. This commentary also reviews mechanisms of IGF-1 function and provides a graphic representation of IGF-1 signaling mechanisms in potential crosstalk relations with mediators of inflammation in the heart (specifically tumor necrosis factor-alpha).
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Wang et al. (2003) conducted a review in Myocardial ischemia/reperfusion injury. Insulin-like growth factor-1 (IGF-1) was evaluated. Insulin-like growth factor-1 confers cardiac protection against ischemia via mitochondria-dependent mechanisms, though long-term exposure may enhance inflammatory responses.
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