Engagement of the innate immune system and activation of inflammatory responses have been demonstrated to play an important role in myocardial ischemia/reperfusion (I/R) injury (Barry 1994; Bryant et al. 1998; Frangogiannis 2006; Kubota et al. 1997) and congestive heart failure (CHF) (Torre-Amione et al. 1996). Experimental studies and clinical investigations have shown that I/R significantly increases myocardial inflammatory cytokine expression including TNF-α, IL-1β, IL-6, IL-8, interferon-γ (IFN-γ), and intercellular adhesion molecule-1 (I-CAM-1) (Barry 1994; Bryant et al. 1998; Frangogiannis 2006; Kubota et al. 1997; Kukielka et al. 1995). These proinflammatory cytokines are directly involved in the progression of myocardial I/R injury, myocardial dysfunction, vascular wall remodeling, and heart failure (Kelly and Smith 1997; Ono et al. 1998). However, we still do not fully understand the mechanisms by which the innate immune and inflammatory responses are involved in ischemic heart diseases.
| Identifer | oai:union.ndltd.org:ETSU/oai:dc.etsu.edu:etsu-works-15664 |
| Date | 01 January 2013 |
| Creators | Ha, Tuanzhu, Liu, Li, Kelley, Jim, Williams, David, Li, Chuanfu |
| Publisher | Digital Commons @ East Tennessee State University |
| Source Sets | East Tennessee State University |
| Detected Language | English |
| Type | text |
| Source | ETSU Faculty Works |
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