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Mentions: NFκB is activated in the heart in many conditions, where the outcome for heart function and cell viability is not clarified and probably not uniform, summarized in the cartoon of Fig. 2. NFκB is activated in the heart during acute ischaemia and reperfusion [36–38]. NFκB is also activated in the heart  and in circulating white blood cells  during unstable angina. Blocking of NFκB reduces ischaemia–reperfusion injury in experimental studies with short times of observation [41–43]. NFκB is activated in the heart by preconditioning, where it is suggested to play a beneficial role for adaptation to ischaemia [34, 35, 39]. Wong et al.  showed for the first time that NFκB was activated in cardiomyocytes in failing hearts of patients with ischaemic heart disease, while similarly an increased NFκB expression was present in the fibrotic areas in patients with dilated cardiomyopathy. Later studies have confirmed that NFκB and its target genes are activated in cardiomyocytes of patients with failing hearts of various etiologies [45, 46] and that the same is the case in mouse and rat models of heart failure . Interestingly, NFκB is also activated in peripheral white blood cells in patients with failure, except in cachectic patients [47, 48]. Furthermore, fatigued skeletal muscle in heart failure patients has increased NFκB activation . Thus, although it is sure that NFκB is activated in human and animal myocardium during remodelling, the relationship between heart and periphery is far from clarified.Fig. 2
Innate immunity and remodelling
Bottom Line: Nuclear factor kappa B regulates gene programmes involved in inflammation as well as the resolution of inflammation.The impact of activation of cardiac innate immunity on the long-term outcome in in vivo models of hypertrophy and remodelling is less clear, with conflicting results as to whether it is beneficial or detrimental.More research using genetically engineered mice as tools, different models of evoking remodelling, and long-term follow-up is required for us to conclude whether activation of the innate immune system is good, bad, or unimportant in chronic injury models.
Affiliation: Department of Physiology, Institute of Basic Medical Sciences, University of Oslo, Postbox 1103 Blindern, 0317, Oslo, Norway. email@example.com
Abstract: A wide variety of cardiac disease states can induce remodelling and lead to the functional consequence of heart failure. These complex disease states involve a plethora of parallel signal transduction events, which may be associated with tissue injury or tissue repair. Innate immunity is activated in hearts injured in different ways, evident as cytokine release from the heart, activation of toll-like receptors involved in recognizing danger, and activation of the transcription factor nuclear factor kappa B. Nuclear factor kappa B regulates gene programmes involved in inflammation as well as the resolution of inflammation. The impact of this is an enigma; while cytokines, toll-like receptors, and nuclear factor kappa B appear to elicit myocardial protection in studies of preconditioning, the literature strongly indicates a detrimental role for activation of innate immunity in studies of acute ischaemia-reperfusion injury. The impact of activation of cardiac innate immunity on the long-term outcome in in vivo models of hypertrophy and remodelling is less clear, with conflicting results as to whether it is beneficial or detrimental. More research using genetically engineered mice as tools, different models of evoking remodelling, and long-term follow-up is required for us to conclude whether activation of the innate immune system is good, bad, or unimportant in chronic injury models.
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