title: Mimicking the endogenous current of injury improves post-infarct cardiac remodeling.
abstract: Myocardial ischemia/reperfusion and infarction (I/R/I) is a leading cause of morbidity and mortality worldwide. The development of effective interventions for I/R/I has had only limited success due to the complex pathological processes of primary and secondary injury that follow I/R/I. Primary injury consists of cell death induced by the ischemic insult. Secondary injury results from activation of inflammatory processes that can induce secondary damage by apoptosis, lipid peroxidation, oxidative stress, or free radical formation. Thus the inflammatory and reparative response, after I/R/I, involves a complex, tightly controlled, and regulated cascade of events that lead to a replacement of the necrotic tissue with a collagen-rich scar. Timely activation and suppression of the inflammatory cascade and regulation of the reparative process is critical to prevent excessive tissue degradation, infarct expansion and heart failure. Accordingly, interventions that physiologically adjust the delicate balance between the essential and detrimental facets of inflammation are expected to provide new therapeutic opportunities. In this context, injury currents are endogenous, physiological mechanisms by which electrical fields interact with the innate immune system to modulate and restrain the inflammatory cascade and promote the reparative process. Accordingly, application of low intensity direct current (LIDC), by placing electrodes directly on the heart, and mimicking the current of injury is expected to enhance the complex biological mechanism of wound healing.
authors.affiliation: Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201, United States.
authors.forename: Heidi L
authors.initials: HL
authors.lastname: Lujan
authors.forename: Stephen E
authors.initials: SE
authors.lastname: DiCarlo
mesh_terms: D004558:Electric Stimulation; D004574:Electromagnetic Fields; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000503:physiopathology*; D008954:Models, Biological; D009203:Myocardial Infarction / Q000150:complications / Q000503:physiopathology*; D020257:Ventricular Remodeling / Q000502:physiology*; D014945:Wound Healing / Q000502:physiology*