Tuning in to the 'right' calcium channel regulation in experimental models of diabetes

Research output: Contribution to journalComment/debate

2 Scopus citations

Abstract

Elucidation of cellular and molecular mechanisms underlying vascular disease is of fundamental importance to the development of pharmacological agents to target these pathways. Pinho et al. in this issue of the BJP provide highly compelling evidence that the δ isoform of phosphatidyl inositol 3-kinase (PI3K δ) was upregulated and accounted for the increase in L-type, voltage-gated, Ca channel current in aortic vascular smooth muscle (VSM) cells of a mouse model of type 1 diabetes. There are several key issues of broad fundamental significance to this work. Firstly, what is the 'right' answer about calcium channel regulation in diabetes? Conflicting reports of increased and decreased Ca channel current may be due to specificity of the vascular bed and species. Then, the time course of diabetic vasculopathy may influence the expression of contractile versus proliferative phenotypes of VSM. Also the metabolic characterization of diabetes may enlighten or confound any study of diabetic vascular disease. These issues need attention to move forward work in this area. LINKED ARTICLE This article is a commentary on Pinho et al., pp. 1458-1471 of this issue. To view this paper visit

Original languageEnglish (US)
Pages (from-to)1455-1457
Number of pages3
JournalBritish Journal of Pharmacology
Volume161
Issue number7
DOIs
StatePublished - Dec 1 2010

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Keywords

  • Catabolism
  • Diabetes
  • Glucose
  • Glucose regulation
  • Metabolism
  • Mouse
  • Phosphatidyl inositol 3-kinase
  • Pig
  • Vascular smooth muscle
  • Voltage-gated calcium channel

ASJC Scopus subject areas

  • Pharmacology

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