A metabolomics-driven approach reveals metabolic responses and mechanisms in the rat heart following myocardial infarction

Int J Cardiol. 2017 Jan 15:227:239-246. doi: 10.1016/j.ijcard.2016.11.127. Epub 2016 Nov 11.

Abstract

Background: Myocardial infarction (MI) is caused by myocardial necrosis resulting from prolonged ischemia. However, the biological mechanisms underlying MI remain unclear.

Methods: We evaluated metabolic and lipidomic changes in rat heart tissue from sham and MI at 1h, 1day and 10day after coronary ligation, using global profiling based on metabolomics.

Results: A time-dependent increase or decrease in polar and lipid metabolite levels was measured. The S-adenosylmethionine (SAM) concentration and the SAM/S-adenosylhomocysteine (SAH) ratio gradually decreased in a time-dependent manner and were significantly downregulated 10days after MI. Transcriptome analysis revealed that the levels of coenzyme Q (Coq)-3 and Coq5, both of which are SAM-dependent methyltransferases, were decreased in the MI groups. These results suggested that dysregulation of SAM may be related to down regulated COQ biosynthetic pathway. In addition, short-chain (C3) and medium-chain (C4-C12) acylcarnitine levels gradually decreased, whereas long-chain acylcarnitine (C14-18) levels increased, owing to a defect in β-oxidation during ischemia. These changes are related to energy-dependent metabolic pathways, and a subsequent decrease in adenosine triphosphate concentration was observed.

Conclusions: The comprehensive integration of various omics data provides a novel means of understanding the underlying pathophysiological mechanisms of MI.

Keywords: Integrative omics analysis; Lipidomics; Metabolomics; Myocardial infarction; Transcriptomics.

MeSH terms

  • Animals
  • Disease Models, Animal
  • Ligation
  • Male
  • Metabolomics*
  • Myocardial Infarction / metabolism*
  • Myocardial Infarction / pathology*
  • Rats
  • Rats, Sprague-Dawley
  • Time Factors