Regulators of necroinflammation in acute kidney injury

Hans-Joachim Anders; Joachim Andrassy; Julia Lichtnekert

doi:10.1016/j.kint.2023.10.019

Regulators of necroinflammation in acute kidney injury

Kidney Int. 2024 Jan;105(1):22-25. doi: 10.1016/j.kint.2023.10.019.

Authors

Hans-Joachim Anders¹, Joachim Andrassy², Julia Lichtnekert³

Affiliations

¹ Renal Division, Department of Medicine IV, University Hospital of the Ludwig Maximilian University, Munich, Germany. Electronic address: [email protected].
² Division of General, Visceral, Vascular and Transplant Surgery, Hospital of Ludwig Maximilians University, Munich, Germany.
³ Renal Division, Department of Medicine IV, University Hospital of the Ludwig Maximilian University, Munich, Germany.

PMID: 38182296
DOI: 10.1016/j.kint.2023.10.019

Abstract

Interleukin (IL)-22 is unique among the ILs as it elicits direct effects on kidney epithelia and regulates cell survival in a context-dependent manner. Studies published in Kidney International and other journals demonstrate opposing roles of IL-22 (e.g., in models of acute kidney injury). In the early necroinflammation phase of acute kidney injury, IL-22 promotes tubular cell death, whereas it enhances the proliferation and regeneration of epithelial barrier function in the healing phase of injured tubules.

Publication types

Research Support, Non-U.S. Gov't
Comment

MeSH terms

Acute Kidney Injury* / etiology
Cell Death
Cell Survival
Epithelial Cells
Humans
Kidney