The ability of the myocardium to successfully compensate for and adapt to stress, ultimately determines whether the heart will decompensate and fail, or whether instead it will maintain preserved function. Despite the importance of the myocardial response to environmental stress, very little is known with respect to the biochemical mechanisms that are responsible for mediating and integrating the stress response in the heart. In the present review we will summarize recent experimental material which suggests that tumor necrosis factor-alpha (TNF-alpha), a pro-inflammatory cytokine that has been identified consistently in virtually all forms of cardiac injury, may play an important role in mediating and integrating the myocardial response to stress. The theme that will emerge from this discussion is that the short-term expression of TNF-alpha within the heart may provide the heart with an adaptive response to stress, whereas long-term expression of TNF-alpha may be frankly maladaptive by producing cardiac decompensation.
- Heat shock protein