Endothelial dysfunction and impaired vascular relaxation represent a common cause of microvascular disease in patients with diabetes. Although multiple mechanisms underlying altered endothelial cell function in diabetes have been described, there is currently no specific and approved pharmacological treatment. In this edition of Clinical Science, Morales-Cano et al. characterize voltage-dependent K+ (Kv) channels as genes regulated by pharmacological activation of peroxisome proliferator-activated receptor-b/d (PPARb/d). Diabetes altered Kv channel function leading to impaired coronary artery relaxation, which was prevented by pharmacological activation of PPARb/d. These studies highlight an important mechanism of vascular dysfunction in diabetes and point to a potential approach for therapy, particularly considering that PPARb/d ligands have been developed and tested in small clinical trials.
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October 2016
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Targeted cancer treatment. In this issue, Gopal et al, review the molecular mechanisms of vascular complications of targeted cancer therapies. See pp. 1763–1779 for further details.Close Modal
Commentary|
September 15 2016
Vascular smooth muscle cell dysfunction in diabetes: nuclear receptors channel to relaxation
Geneviève Doyon;
Geneviève Doyon
*Division 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.
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Dennis Bruemmer
*Division 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.
Correspondence: Dennis Bruemmer (email bruemmerd@upmc.edu).
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Clin Sci (Lond) (2016) 130 (20): 1837–1839.
Article history
Received:
July 11 2016
Revision Received:
August 04 2016
Accepted:
August 08 2016
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Geneviève Doyon, Dennis Bruemmer; Vascular smooth muscle cell dysfunction in diabetes: nuclear receptors channel to relaxation. Clin Sci (Lond) 1 October 2016; 130 (20): 1837–1839. doi: https://doi.org/10.1042/CS20160518
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