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Related Experiment Video

Updated: Nov 20, 2025

A Zebrafish Model of Diabetes Mellitus and Metabolic Memory
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Endothelial cell metabolic memory causes cardiovascular dysfunction in diabetes.

Yufeng Yao1, Qixue Song1, Changqing Hu2

  • 1Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology and Center for Human Genome Research, Huazhong University of Science and Technology, 1037 Luoyu Road, Wuhan, P. R. China.

Cardiovascular Research
|January 23, 2021
PubMed
Summary

High blood sugar causes lasting damage in blood vessel cells, leading to heart problems in diabetes. Blocking this "metabolic memory" with specific treatments can restore heart function.

Keywords:
(Smad2 and Smad3)Cardiac perivascular fibrosisDiabetes mellitusEndMTEndothelial cellMetabolic memoryNF-κB (p65)NRF2TGF-βmiR-27a-3pmiR-29

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Area of Science:

  • Cardiovascular Science
  • Molecular Biology
  • Endocrinology

Background:

  • Diabetes is associated with cardiovascular dysfunction, partly due to endothelial cell (EC) damage.
  • Hyperglycaemia-induced metabolic memory in ECs contributes to long-term cardiovascular complications.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying hyperglycaemia-induced metabolic memory in ECs.
  • To demonstrate the role of EC metabolic memory in the development of diabetic cardiovascular dysfunction.

Main Methods:

  • Investigated signalling pathways including NF-κB, NRF2, and TGF-β in ECs under high glucose conditions.
  • Utilized a miR-27a-3p inhibitor and an NRF2 activator (tert-butylhydroquinone) to block metabolic memory effects.
  • Assessed in vivo effects in streptozotocin-induced diabetic mice, evaluating cardiac fibrosis and function.

Main Results:

  • Hyperglycaemia induced a "metabolic memory" in ECs, characterized by sustained NF-κB signaling, miR-27a-3p upregulation, NRF2 downregulation, TGF-β activation, and EndMT.
  • This EC metabolic memory persisted even after glucose normalization, leading to perivascular fibrosis and cardiac dysfunction.
  • NRF2 activation and miR-27a-3p inhibition effectively blocked these detrimental EC memory effects.
  • In vivo, these interventions restored cardiac function and reduced fibrosis in diabetic mice, unlike insulin alone.

Conclusions:

  • Disrupting hyperglycaemia-induced EC metabolic memory is crucial for restoring cardiac function in diabetes treatment.
  • Identified a novel molecular pathway (NF-κB/miR-27a-3p/NRF2/ROS/TGF-β/EndMT) driving EC metabolic memory and cardiovascular dysfunction.