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Related Concept Videos

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Related Experiment Video

Updated: May 12, 2025

Delivery of Exogenous Artificially Synthesized miRNA Mimic to the Kidney Using Polyethylenimine Nanoparticles in Several Kidney Disease Mouse Models
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Engineered Neuromedin U Promotes Type 2 Innate Immunity and Renoprotection in Acute Kidney Injury.

Sara Trindade-Correia1,2,3, Vasco Correia1, Filipe Delgado1

  • 1LiMM Therapeutics, Lisboa, Portugal.

Journal of the American Society of Nephrology : JASN
|May 8, 2025
PubMed
Summary

An engineered neuromedin U analogue, LIMM102, shows therapeutic potential for acute kidney injury (AKI). This treatment improved kidney function and survival in a preclinical model by activating type 2 innate lymphoid cells (ILC2s) via NMUR1 signaling.

Keywords:
AKIimmunologyischemia-reperfusionlymphocytestransgenic mouse

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Area of Science:

  • Nephrology
  • Immunology
  • Pharmacology

Background:

  • Acute kidney injury (AKI) is a critical condition characterized by sudden kidney function loss.
  • Type 2 innate lymphoid cells (ILC2s), activated by neuromedin U (NMU), play a role in tissue repair and homeostasis.
  • Renal ILC2s have demonstrated protective effects in AKI models.

Purpose of the Study:

  • To investigate the therapeutic efficacy of LIMM102, an engineered NMU analogue, in a preclinical model of renal ischemia-reperfusion injury (IRI)-induced AKI.
  • To determine the mechanism underlying LIMM102's effects, specifically its reliance on NMUR1 signaling and ILC2 activation.

Main Methods:

  • Administration of LIMM102 to wild-type mice subjected to IRI-induced AKI.
  • Assessment of survival rates, glomerular filtration rate (GFR), kidney function biomarkers, and histopathology.
  • Evaluation of LIMM102's efficacy in NMUR1-deficient mice to confirm the necessity of NMUR1 signaling.

Main Results:

  • LIMM102 treatment significantly reduced mortality rates in IRI-induced AKI mice.
  • LIMM102 administration improved GFR, lowered kidney injury biomarkers, and reduced lesion severity.
  • Therapeutic benefits of LIMM102 were dependent on NMUR1 signaling, as evidenced by the lack of effect in Nmur1-deficient mice.

Conclusions:

  • LIMM102 demonstrates significant renoprotective effects in IRI-induced AKI.
  • The therapeutic action of LIMM102 is mediated through NMUR1 signaling and is associated with the activation of renal ILC2s.