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Vascular smooth muscle cell dysfunction in diabetes: nuclear receptors channel to relaxation

Geneviève Doyon1, Dennis Bruemmer2

  • 1Division of Cardiology, Department of Medicine, Pittsburgh Heart, Lung, Blood, and Vascular Medicine Institute, UPMC and University of Pittsburgh School of Medicine Pittsburgh, PA 15261, U.S.A.

Clinical Science (London, England : 1979)
|September 17, 2016
PubMed

Insights

Diabetes impairs blood vessel function by altering voltage-dependent K(+) (Kv) channels. Activating peroxisome proliferator-activated receptor-b/d (PPARb/d) protected against this dysfunction, suggesting a potential therapy for diabetic vascular disease.

Area of Science:

  • Cardiovascular Biology
  • Endocrinology
  • Molecular Medicine

Background:

  • Endothelial dysfunction and impaired vascular relaxation are hallmarks of microvascular disease in diabetes.
  • Existing research has identified several mechanisms for altered endothelial cell function in diabetes, but specific pharmacological treatments are lacking.

Purpose of the Study:

  • To characterize voltage-dependent K(+) (Kv) channels as genes regulated by peroxisome proliferator-activated receptor-b/d (PPARb/d) activation.
  • To investigate the role of Kv channels in diabetes-induced vascular dysfunction.
  • To explore the therapeutic potential of PPARb/d activation in mitigating diabetic vascular complications.

Main Methods:

  • Pharmacological activation of PPARb/d.
  • Assessment of Kv channel function in diabetic models.
  • Measurement of coronary artery relaxation.

Main Results:

  • Diabetes altered Kv channel function, contributing to impaired coronary artery relaxation.
  • Pharmacological activation of PPARb/d prevented the diabetes-induced alterations in Kv channel function and restored normal coronary artery relaxation.

Conclusions:

  • Kv channels are key mediators of vascular dysfunction in diabetes.
  • Pharmacological activation of PPARb/d represents a promising therapeutic strategy for diabetic vascular disease.
  • PPARb/d ligands warrant further investigation for clinical application in managing diabetic complications.

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