Galectin-3 mediates cardiac remodeling caused by impaired glucose and lipid metabolism through inhibiting two pathways of activating Akt
Zhen Sun, Lili Zhang, Lihua Li, Chen Shao, Jia Liu, Mengxue Zhou, Zhongqun Wang
Abstract
Studies on the pathogenesis of diabetic cardiac remodeling are highly desired. Glucose and lipid metabolism are both disordered in diabetes. Glucose and lipid metabolism disturbances promote myocardial fibrosis, apoptosis, and hypertrophy through galectin-3. Galectin-3 promotes cardiac remodeling by inhibiting phosphorylation of Akt Thr308 or Akt Ser473 . The present study finds that glucose and lipid metabolism disorders are important causes for myocardial damage and provides novel ideas for the prevention and treatment of diabetic cardiac remodeling.
Topics & Concepts
Protein kinase BPI3K/AKT/mTOR pathwayLipid metabolismFibrosisAMPKInternal medicineEndocrinologyPhosphorylationCardiac fibrosisSignal transductionApoptosisBiologyMedicineCancer researchCell biologyProtein kinase ABiochemistryGalectins and Cancer BiologySignaling Pathways in DiseaseProtein Tyrosine Phosphatases