G protein-linked cell signaling and cardiovascular functions in diabetes/hyperglycemia

Shehla Hashim1, Yuan Li, Madhu B Anand-Srivastava

  • 1Department of Physiology and Groupe de recherche sur le système nerveux autonome (GRSNA), Faculty of Medicine, University of Montreal, Montreal, Quebec, Canada.

Insights

Diabetes complications like impaired vascular function stem from chronic hyperglycemia. This review explores how G protein-linked cell signaling pathways are altered, contributing to these vascular issues in diabetes.

Area of Science:

  • Cardiovascular Biology
  • Endocrinology
  • Molecular Signaling

Background:

  • Vascular complications, including impaired contractility and increased cell proliferation, are common in diabetes.
  • Chronic hyperglycemia is a key contributor to these adverse vascular effects.

Purpose of the Study:

  • To review the various G protein-linked cell signaling pathways affected by diabetes and hyperglycemia.
  • To discuss the implications of these signaling pathway alterations on vascular function.

Main Methods:

  • Literature review of studies investigating cellular and molecular mechanisms in diabetes-induced vascular dysfunction.
  • Analysis of signaling pathways including nonenzymatic glycation, protein kinase C (PKC), oxidative stress, and G protein-adenylyl cyclase signaling.

Main Results:

  • Hyperglycemia affects vascular smooth muscle cells via pathways like PKC activation and oxidative stress.
  • G protein-coupled adenylyl cyclase/cAMP and phospholipase C/PKC pathways are implicated in hyperglycemia-induced L-type Ca2+ channel stimulation.
  • Hyperglycemia reduces nitric oxide availability and impairs G protein-adenylyl cyclase signaling.

Conclusions:

  • Dysregulation of G protein-linked cell signaling pathways is a significant factor in diabetes-related vascular complications.
  • Understanding these pathways is crucial for developing therapeutic strategies to manage diabetic vascular disease.

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