Ryanodine receptor and immune-related molecules in diabetic cardiomyopathy

Cheng-Ju Tian1, Jing-Hua Zhang2, Jinfeng Liu3

  • 1College of Rehabilitation and Sports Medicine, Jinzhou Medical University, Jinzhou, China.

ESC Heart Failure
|May 20, 2021
PubMed

Insights

High blood sugar (hyperglycaemia) damages the heart, causing diabetic cardiomyopathy. This review explores how ryanodine receptors (RyRs) and immune signals interact to cause heart dysfunction and potential therapies.

Area of Science:

  • Cardiovascular Biology
  • Metabolic Disease Research
  • Molecular Cardiology

Background:

  • Hyperglycaemia is a primary driver of diabetic cardiomyopathy.
  • It elevates reactive species (RCS, ROS, RNS), disrupts calcium balance, and promotes inflammation.
  • Ryanodine receptor 2 (RyR2) is crucial for cardiac excitation-contraction coupling.

Purpose of the Study:

  • To review new findings on cellular communication in diabetic cardiomyopathy.
  • To elucidate the mechanistic link between RyRs and immune molecules in diabetes.
  • To discuss therapeutic strategies targeting RyRs and immune pathways.

Main Methods:

  • Literature review focusing on recent advancements.
  • Analysis of post-translational modifications of RyRs.
  • Examination of immune signaling pathways (e.g., IL-1) in cardiac disease.

Main Results:

  • Post-translational modifications of RyRs by reactive species impair gating and calcium sensitivity.
  • Cardiac inflammation, involving lymphocytes and IL-1, contributes to diabetic cardiomyopathy.
  • Complex intercellular communication networks among cardiomyocytes, fibroblasts, and immune cells are implicated.

Conclusions:

  • Dysregulation of RyRs and immune molecules are key in diabetic cardiomyopathy pathogenesis.
  • Understanding these interactions offers novel therapeutic targets for diabetic heart complications.

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