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Identification of the Source of Secreted Proteins in the Kidney by Brefeldin A Injection
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Regulation and function of CX3CR1 and its ligand CX3CL1 in kidney disease

Sibylle von Vietinghoff1,2, Christian Kurts3

  • 1First Medical Clinic, Nephrology Section, University Clinic of the Rheinische Friedrich Wilhelms University Bonn, Venusberg Campus 1, 53127, Bonn, Germany. Sibylle.von_Vietinghoff@uk-bonn.de.

Cell and Tissue Research
|May 19, 2021
PubMed

Insights

The chemokine CX3CL1 (fractalkine) and its receptor CX3CR1 are key regulators of leukocyte behavior in the kidney. Their dysregulation is implicated in various kidney diseases and systemic inflammation.

Area of Science:

  • Nephrology
  • Immunology
  • Molecular Biology

Background:

  • Leukocyte trafficking to the kidney is regulated by chemokines.
  • CX3CL1 (fractalkine) and its receptor CX3CR1 are highly expressed in kidney diseases.
  • CX3CL1 is produced by renal endothelium and tubular epithelium, attracting leukocytes.

Purpose of the Study:

  • To review the role and regulatory mechanisms of the CX3CL1-CX3CR1 axis in kidney inflammation.
  • To discuss the involvement of CX3CR1+ myeloid cells in kidney damage.
  • To explore the systemic effects of CX3CL1-CX3CR1 in renal impairment.

Main Methods:

  • Review of existing literature on CX3CL1 and CX3CR1 in kidney diseases.
  • Analysis of experimental models of kidney inflammation.
  • Examination of clinical data on CX3CR1+ monocytes in renal impairment.

Main Results:

  • CX3CR1 is essential for myeloid cell homing to the kidney in homeostasis and inflammation.
  • The CX3CL1-CX3CR1 axis is dysregulated in IgA nephritis, lupus erythematosus, and transplant rejection.
  • CX3CR1+ myeloid cells contribute to contrast-agent and sepsis-induced kidney damage.

Conclusions:

  • The CX3CL1-CX3CR1 axis plays a critical role in localized and systemic renal inflammation.
  • Understanding this axis offers potential therapeutic targets for kidney diseases.
  • CX3CR1+ monocyte levels may serve as a biomarker for renal impairment and cardiovascular risk.

Keywords:
Cell migrationChemokinesDiabetic nephropathyGlomerulonephritisHyperthensionLPSMacrophagesPodocytesPyelonephritisTubular epithelial cells

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