Immune mechanisms in the different phases of acute tubular necrosis

Fedor Kundert; Louise Platen; Takamasa Iwakura; Zhibo Zhao; Julian A. Marschner; Hans-Joachim Anders

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자료유형: 학술저널

저자정보: Fedor Kundert (Klinikum der Universität München) Louise Platen (Klinikum der Universität München) Takamasa Iwakura (Klinikum der Universität München) Zhibo Zhao (Klinikum der Universität München) Julian A. Marschner (Klinikum der Universität München) Hans-Joachim Anders (Klinikum der Universität München)

저널정보: 대한신장학회 Kidney Research and Clinical Practice Kidney Research and Clinical Practice Vol.37 No.3

발행연도: 2018.1

수록면: 185 - 196 (12page)

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Acute kidney injury is a clinical syndrome that can be caused by numerous diseases including acute tubular necrosis (ATN). ATN evolves in several phases, all of which are accompanied by different immune mechanisms as an integral component of the disease process. In the early injury phase, regulated necrosis, damage-associated molecular patterns, danger sensing, and neutrophil-driven sterile inflammation enhance each other and contribute to the crescendo of necroinflammation and tissue injury. In the late injury phase, renal dysfunction becomes clinically apparent, and M1 macrophage-driven sterile inflammation contributes to ongoing necroinflammation and renal dysfunction. In the recovery phase, M2-macrophages and anti-inflammatory mediators counteract the inflammatory process, and compensatory remnant nephron and cell hypertrophy promote an early functional recovery of renal function, while some tubules are still badly injured and necrotic material is removed by phagocytes. The resolution of inflammation is required to promote the intrinsic regenerative capacity of tubules to replace at least some of the necrotic cells. Several immune mechanisms support this wound-healing-like re-epithelialization process. Similar to wound healing, this response is associated with mesenchymal healing, with a profound immune cell contribution in terms of collagen production and secretion of pro-fibrotic mediators. These and numerous other factors determine whether, in the chronic phase, persistent loss of nephrons and hyperfunction of remnant nephrons will result in stable renal function or progress to decline of renal function such as progressive chronic kidney disease.

참고문헌 (112)

참고문헌 신청

Mehta RL / 2007 / Acute kidney injury network: report of an initiative to improve outcomes in acute kidney injury / Crit Care 11:R31

Khwaja A / 2012 / KDIGO clinical practice guidelines for acute kidney injury / Nephron Clin Pract 120:c179~c184

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