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01.06.2016 | Schwerpunkt ERA-EDTA
Mediators of necroinflammation in kidney disease
Erschienen in: Wiener klinisches Magazin | Ausgabe 3/2016
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Known since ancient times: tissue injury and inflammation often go together but what are the underlying molecular mechanisms? Inflammation triggers cell death via complement activation or cytotoxic T cells. Dying cells release molecules that trigger inflammation by activating pattern recognition receptors (PRR) of the innate immune system. This bidirectional relationship between inflammation and cell necrosis fuelling an autoamplification loop is referred to as necroinflammation (Fig. 1; [5]). Necroinflammation is accelerated by immunity-related cell necrosis and cell necrosis-related immune activation. Necroinflammation can be initiated by a few necrotic cells that activate the innate immune system, which subsequently leads to necrosis of more cells triggering more inflammation, a process that can eventually lead to organ failure (Fig. 1).×
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