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Updated: Jul 13, 2026

Mouse Electroacupuncture Fixation Device Fabrication for Electroacupuncture Pretreatment in Diabetic Cardiomyopathy Mouse Model
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Mouse Electroacupuncture Fixation Device Fabrication for Electroacupuncture Pretreatment in Diabetic Cardiomyopathy Mouse Model

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S100A8/S100A9 Links Diabetic Stress to Cardiac Progenitor Cell Dysfunction and Fibrotic Heart Failure: An Integrated

Yang Yang1, Ge Cao2

  • 1Department of Critical Care Medicine, West China Hospital, Sichuan University/West China School of Nursing, Sichuan University, Chengdu, Sichuan, China, scu.edu.cn.

Human Mutation
|July 12, 2026
PubMed
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Diabetic heart failure involves S100A8/S100A9, which links high blood sugar to oxidative stress, metabolic issues, and fibrosis in cardiac progenitor cells. This protein complex may be a key biomarker and therapeutic target.

Area of Science:

  • Cardiovascular Biology
  • Metabolic Disease Research
  • Molecular Medicine

Background:

  • Diabetes significantly elevates heart failure risk, but the underlying molecular mechanisms connecting metabolic dysfunction, fibrosis, and poor cardiac repair are not fully understood.
  • Identifying specific molecular signals is crucial for understanding and treating diabetic cardiomyopathy.

Purpose of the Study:

  • To identify key molecular mediators in diabetic heart failure by integrating multi-omics data and pathway analyses.
  • To investigate the role of identified mediators in cardiac progenitor cells (CPCs) and their potential as therapeutic targets.

Main Methods:

  • Integrated transcriptomic, gene, and protein-protein interaction data from diabetic and nondiabetic heart failure models.
  • Utilized single-cell RNA sequencing to map gene expression in specific cardiac cell types.
Keywords:
biomarkersdiabetes mellitusheart failureoncologyprognosis

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Last Updated: Jul 13, 2026

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Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model
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Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model

Published on: November 29, 2024

  • Performed mechanistic studies in human CPCs under varying glucose conditions, including gene knockdown/overexpression and antibody neutralization, assessing cell viability, gene expression, oxidative stress, and mitochondrial function.

    • Main Results:

    • S100A8 was identified as a fibrosis-related hub protein predominantly expressed in CPCs in diabetic heart failure.
    • High glucose conditions upregulated S100A8/S100A9 in CPCs, promoting profibrotic and proinflammatory gene expression, increasing oxidative stress, and impairing mitochondrial respiration.
    • S100A9 manipulation demonstrated its causal role in CPC dysfunction, with neutralization attenuating negative effects; high S100A8 expression correlated with poor prognosis in cancer cohorts.

    Conclusions:

    • S100A8/S100A9 acts as a critical mediator linking hyperglycemia, oxidative stress, metabolic inflexibility, and fibrotic reprogramming in CPCs, driving diabetic heart failure.
    • S100A8/S100A9 represents a potential biomarker and therapeutic target at the intersection of immunometabolism, cardiac regeneration, and oncology.