Diabetes-induced changes in cardiac voltage-gated ion channels


Ozturk N., USLU S., ÖZDEMİR S.

WORLD JOURNAL OF DIABETES, cilt.12, sa.1, ss.1-18, 2021 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Derleme
  • Cilt numarası: 12 Sayı: 1
  • Basım Tarihi: 2021
  • Doi Numarası: 10.4239/wjd.v12.i1.1
  • Dergi Adı: WORLD JOURNAL OF DIABETES
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), EMBASE
  • Sayfa Sayıları: ss.1-18
  • Anahtar Kelimeler: Diabetes, Action potential, Cardiac ion channels, L-type Ca2+ channels, Potassium channels, Sodium channels, RECTIFIER K+-CURRENT, PERSISTENT SODIUM CURRENT, ABNORMAL QT PROLONGATION, VENTRICULAR MYOCYTES, POTASSIUM-CHANNEL, HEART-FAILURE, CALCIUM-CHANNEL, GENE-EXPRESSION, SIGNALING CONTRIBUTES, INTERVAL PROLONGATION
  • Akdeniz Üniversitesi Adresli: Evet

Özet

Diabetes mellitus affects the heart through various mechanisms such as microvascular defects, metabolic abnormalities, autonomic dysfunction and incompatible immune response. Furthermore, it can also cause functional and structural changes in the myocardium by a disease known as diabetic cardiomyopathy (DCM) in the absence of coronary artery disease. As DCM progresses it causes electrical remodeling of the heart, left ventricular dysfunction and heart failure. Electrophysiological changes in the diabetic heart contribute significantly to the incidence of arrhythmias and sudden cardiac death in diabetes mellitus patients. In recent studies, significant changes in repolarizing K+ currents, Na+ currents and L-type Ca2+ currents along with impaired Ca2+ homeostasis and defective contractile function have been identified in the diabetic heart. In addition, insulin levels and other trophic factors change significantly to maintain the ionic channel expression in diabetic patients. There are many diagnostic tools and management options for DCM, but it is difficult to detect its development and to effectively prevent its progress. In this review, diabetes-associated alterations in voltage-sensitive cardiac ion channels are comprehensively assessed to understand their potential role in the pathophysiology and pathogenesis of DCM.