| description abstract | Cells can launch self-protective mechanisms against injury, induced by ischemia, mechanical impact, toxins, radiation, or microorganisms (viruses, bacteria, and fungi), and can also recruit other cells to assist in the protective processes. Primary cell protective mechanisms include early-phase discharge of small molecules (adenosine and bradykinin) and subsequent expression and release of cytokines, growth factors, and anti-reactive oxygen species enzymes from the injured cells as well as activated/recruited cells. These protective factors can act on cognate signaling pathways in the injured cells to support cell survival and prevent cell death. However, these cell protective mechanisms are not optimal in the timing of activation and the level of effectiveness—often occurring after cell death with insufficient activity. Thus, it is necessary to develop and utilize cell protective engineering strategies to activate promptly protective factors to sufficient levels, thereby optimizing cell protective processes. This article reviews the molecular mechanisms of cell protection in injury by using experimental myocardial ischemia as a model and potential engineering strategies for optimizing cell protective processes. | |
