A new biomaterial and molecular imaging platform: Click-coupled dual-responsive fluorescent signaling for deciphering

Yongchuang Li1, Haiyue Liu2, Songhan Liu3

  • 1Research Institute of Applied Chemistry, Shanxi University, Taiyuan, 030006, China.

Biomaterials
|August 3, 2026
PubMed

Insights

Researchers developed a new fluorescent probe to simultaneously track glutathione (GSH) and peroxynitrite (ONOO-) in kidney injury. This dual-tracking method reveals how ferroptosis exacerbates renal damage and enables non-invasive diagnosis via urinalysis.

Area of Science:

  • Biomedical Engineering
  • Molecular Biology
  • Renal Pathophysiology

Background:

  • Kidney injury can lead to multi-organ failure, with ferroptosis, a cell death mode, playing a key role.
  • Ferroptosis is driven by redox imbalance, but tracking individual redox events is insufficient to understand kidney injury pathogenesis.
  • Simultaneous monitoring of oxidative and reductive markers is crucial for understanding renal pathogenesis and enabling early intervention.

Purpose of the Study:

  • To engineer a dual-responsive fluorescent probe for simultaneous monitoring of glutathione (GSH) and peroxynitrite (ONOO-) in ferroptosis-mediated kidney injury.
  • To elucidate the dynamic interplay between GSH depletion and ONOO- accumulation in kidney injury models.
  • To validate the probe for real-time in vivo tracking and potential non-invasive diagnostic applications.

Main Methods:

  • Development of a click-coupled dual-responsive fluorescent probe (CY-LS) with hydrophilic chains for synergistic monitoring of GSH and ONOO-.
  • In vivo tracking of GSH and ONOO- dynamics in drug-induced acute and diabetic-induced chronic kidney injury models.
  • Assessment of ferroptosis inhibition effects on redox markers and validation of the probe for therapeutic monitoring.

Main Results:

  • The CY-LS probe enabled real-time, in-situ tracking of GSH and ONOO- dynamics in vivo.
  • Synchronous GSH depletion and ONOO- accumulation were found to synergistically exacerbate kidney injury via ferroptosis.
  • Pharmacological inhibition of ferroptosis reversed the observed redox dyshomeostasis, confirming the probe's utility for therapeutic monitoring.
  • The probe demonstrated exceptional renal clearance, enabling non-invasive diagnosis through urinalysis.

Conclusions:

  • The developed modular toolkit, CY-LS probe, is effective for deciphering renal pathologies driven by ferroptosis.
  • Simultaneous tracking of GSH and ONOO- provides critical insights into redox-driven kidney injury.
  • This approach paves the way for precision diagnosis and therapeutic monitoring of redox-associated disorders.

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