Quantitative Assessment of Ferroptosis in Cardiomyocytes Using Robust and Reliable Electrophysiological Biosensing

Shushan Hua1,2, Shoufang Tong2,3, Yuli Hu4

  • 1Laboratory Medicine Center, Allergy Center, Department of Transfusion Medicine, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou 310014, China.

ACS Sensors
|April 6, 2026
PubMed

Insights

Researchers developed a novel biosensing platform to monitor ferroptosis (iron-dependent cell death) in heart cells. This technology allows for continuous, non-invasive tracking of ferroptosis progression, aiding in understanding cardiac disease and drug development.

Area of Science:

  • Biomedical Engineering
  • Cardiovascular Research
  • Cell Death Mechanisms

Background:

  • Ferroptosis, an iron-dependent cell death, is implicated in cardiovascular diseases due to cardiomyocyte damage from iron overload and lipid peroxidation.
  • Current methods for monitoring ferroptosis are often invasive and lack dynamic, continuous tracking capabilities.
  • Effective monitoring is crucial for understanding cardiac pathogenesis and developing targeted therapies.

Purpose of the Study:

  • To develop a novel biosensing platform for non-invasive, label-free, and quantitative monitoring of cardiomyocyte ferroptosis.
  • To validate the platform's ability to detect electrophysiological signatures associated with ferroptosis.
  • To assess the platform's utility in drug screening and studying ferroptosis-related cardiac conditions.

Main Methods:

  • Development of a custom 32-channel microelectrode array biosensing platform.
  • Non-invasive, label-free electrophysiological monitoring of cardiomyocyte ferroptosis.
  • Induction of ferroptosis using Erastin and assessment of rescue effects with ferrostatin-1.
  • Comparison of detected electrophysiological changes with traditional biochemical assays.

Main Results:

  • The biosensing platform successfully captured dynamic, time- and drug-dependent electrophysiological alterations during Erastin-induced ferroptosis.
  • Detected electrophysiological changes correlated well with traditional biochemical assays, accurately reflecting ferroptosis progression.
  • The platform demonstrated high specificity, successfully recording the rescue effects of ferrostatin-1.

Conclusions:

  • The developed biosensing platform enables the visualization and continuous tracking of cardiomyocyte ferroptosis through electrophysiological monitoring.
  • This technology offers a powerful tool for investigating ferroptosis mechanisms in cardiovascular pathology.
  • The platform shows promise for high-throughput drug screening and the study of ferroptosis-related cardiac diseases.

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