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RETRACTED: Blocking Macrophage Migration Inhibitory Factor Protects Against Cisplatin-Induced Acute Kidney Injury in

Jinhong Li1, Ying Tang2, Patrick M K Tang3

  • 1Department of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, China; Department of Anatomical and Cellular Pathology, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, China; Department of Nephrology, The Seventh Affiliated Hospital of Sun Yat-sen University, Sun Yat-sen University, Shenzhen, China.

Molecular Therapy : the Journal of the American Society of Gene Therapy
|August 6, 2018
PubMed
Abstract

No abstract available in PubMed .

Insights

Macrophage migration inhibitory factor (MIF) is pathogenic in acute kidney injury (AKI). Blocking MIF with an inhibitor (RPS19) protected kidneys in a mouse model, suggesting MIF as a therapeutic target for AKI.

Area of Science:

  • Nephrology
  • Immunology
  • Molecular Biology

Background:

  • Macrophage migration inhibitory factor (MIF) levels are elevated in acute kidney injury (AKI) patients.
  • MIF is a potential predictor for renal replacement therapy in AKI.
  • MIF's pathogenic role in AKI requires further investigation.

Purpose of the Study:

  • To investigate the pathogenic role of MIF in cisplatin-induced AKI.
  • To evaluate MIF as a therapeutic target for AKI.
  • To explore the therapeutic potential of an MIF inhibitor, ribosomal protein S19 (RPS19).

Main Methods:

  • Cisplatin-induced AKI mouse model.
  • Assessment of renal function (serum creatinine) and histology.
  • Measurement of inflammatory markers and immune cell infiltration.
  • Genetic deletion of MIF (MIF-knockout mice).
  • Pharmacological inhibition of MIF using RPS19.

Main Results:

  • Elevated plasma MIF correlated with AKI severity, renal inflammation, and tubular necrosis.
  • MIF deletion significantly improved renal function and reduced inflammation.
  • RPS19 treatment, unlike mutant RPS19, suppressed AKI, mimicking MIF knockout effects.
  • Both genetic and pharmacological MIF inhibition inactivated the CD74-NF-κB signaling pathway.

Conclusions:

  • MIF plays a pathogenic role in cisplatin-induced AKI.
  • Targeting MIF with inhibitors like RPS19 shows therapeutic potential for AKI.
  • Inhibition of the CD74-NF-κB pathway is a key mechanism for MIF's protective effect in AKI.
Keywords:
RPS19acute kidney injurymacrophage migration inhibitory factor

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