Coronary Large Conductance Ca2+-Activated K+ Channel Dysfunction in Diabetes Mellitus

Tong Lu1, Hon-Chi Lee1

  • 1Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, United States.

Frontiers in Physiology
|November 8, 2021
PubMed

Insights

Diabetes mellitus impairs blood vessel function by reducing large conductance Ca2+-activated K+ (BK) channels. This review details the molecular and physiological mechanisms behind this diabetic BK channelopathy.

Area of Science:

  • Cardiovascular Science
  • Endocrinology
  • Molecular Biology

Background:

  • Diabetes mellitus (DM) significantly increases macrovascular and microvascular complication risks.
  • Cardiovascular diseases are a primary cause of mortality in diabetic individuals.
  • Large conductance Ca2+-activated K+ (BK) channels in arteries regulate vascular tone and organ perfusion.

Purpose of the Study:

  • To review the molecular, physiological, and biophysical mechanisms of coronary BK channelopathy in diabetes mellitus.
  • To elucidate how diabetes affects BK channel function and expression in the vasculature.

Main Methods:

  • Literature review of existing research on BK channels in diabetes.
  • Analysis of molecular signaling pathways and transcriptional factors involved.
  • Examination of biophysical properties and protein expression of BK channels.

Main Results:

  • Diabetic vasculopathy is linked to reduced BK channel function, protein expression, and altered biophysical properties.
  • Diabetes-associated signaling pathways and transcription factors contribute to BK channel downregulation.
  • Understanding these mechanisms is crucial for addressing diabetic cardiovascular complications.

Conclusions:

  • Diabetes mellitus induces coronary BK channelopathy through molecular and physiological alterations.
  • Downregulation of BK channels exacerbates vascular dysfunction in diabetic patients.
  • Further research into these mechanisms may reveal therapeutic targets for diabetic cardiovascular disease.

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