Cardiac shock wave therapy promotes arteriogenesis of coronary micrangium, and ILK is involved in the biomechanical effects by proteomic analysis

Sci Rep. 2018 Jan 29;8(1):1814. doi: 10.1038/s41598-018-19393-z.

Abstract

Cardiac Shock Wave Therapy (CSWT) improves myocardial perfusion and ameliorates cardiac remodeling after acute myocardial infarction (AMI), but the precise mechanisms remain obscure. Herein, we have applied CSWT to a rat model of AMI to demonstrate the arteriogenesis of coronary micrangium and protein expression changes in ischemic myocardium after CSWT. Four weeks after CSWT, the fraction shortening of rats was improved greatly and the cardiomyocyte apoptosis index was significantly lower than the AMI group (P < 0.05). Besides, the fibrotic area was markedly decreased in the CSWT group. In the infarction border zone, the thickness of smooth muscle layer was expanded apparently after CSWT. Label-free quantitative proteomic analysis and bioinformatics analysis revealed that the differentially expressed proteins were largely enriched in the focal adhesion signaling pathway. And integrin linked kinase (ILK) may be a key factor contributed to arteriogenesis of coronary micrangium during CSWT. In conclusion, non-invasive cardiac shock wave could promote arteriogenesis of coronary micrangium and alleviate myocardial apoptosis and fibrosis after AMI. Furthermore, focal adhesion signaling pathway may have a central role in the related signal network and ILK was closely related to the arteriogenesis of coronary micrangium during CSWT.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / physiology
  • Extracorporeal Shockwave Therapy / methods
  • Heart / physiology*
  • Male
  • Morphogenesis / physiology*
  • Myocardial Infarction / metabolism
  • Myocardial Infarction / physiopathology
  • Myocardium / metabolism*
  • Protein Serine-Threonine Kinases / metabolism*
  • Proteomics / methods
  • Rats
  • Rats, Sprague-Dawley
  • Signal Transduction / physiology

Substances

  • integrin-linked kinase
  • Protein Serine-Threonine Kinases