Mitochondrial Dynamics in Tachycardiomyopathy

Cell Physiol Biochem. 2019;52(3):435-438. doi: 10.33594/000000031. Epub 2019 Mar 15.


Background/aims: Tachycardiomyopathy (TCM) is a largely reversible form of non-ischemic heart failure. The underlying mechanism are, however, still today poorly understood. Recent data indicate distinct changes in mitochondrial distribution in these patients, compared to other non-ischemic cardiomyopathies.This study investigated underlying mechanisms in mitochondrial dynamics in endomyocardial biopsy samples (EMB) from patients with TCM and compared them to patients with dilated cardiomyopathy (DCM), which show similar clinical features.

Methods: Focused mRNA analyses were performed on routinely obtained paraffinfixed EMB specimen from patients fulfilling TCM diagnosis criteria, as well as patients with DCM to elucidate regulatory changes in mitochondrial fusion, fission and mitophagy.

Results: In patients with TCM we were able to identify mRNA of Mitofusin 1 and 2, two effector proteins regulating mitochondrial fusion, to be strongly upregulated compared to patients with DCM. Conclusively, we did not find differences in the mRNA expression of mitochondrial fission regulators including DRP1, Fis1, MFF, MiD49, and MiD51. Furthermore, we did not find significant changes in PINK1 expression, an important mediator for mitochondrial autophagy.

Conclusion: The mRNA upregulation of Mitofusin 1 and 2 provides first insight into the complex changes of mitochondrial dynamics in cardiomyocytes of patients with reversible heart failure due to TCM.

Keywords: Fusion; Heart failure; Mfn1; Mfn2; Mitochondria; TCM; Tachycardiomyopathy.

MeSH terms

  • Biopsy
  • Cardiomyopathy, Dilated / classification
  • Cardiomyopathy, Dilated / diagnosis
  • Cardiomyopathy, Dilated / genetics*
  • Cardiomyopathy, Dilated / physiopathology
  • Dynamins
  • GTP Phosphohydrolases / genetics*
  • GTP Phosphohydrolases / metabolism
  • Gene Expression Regulation
  • Heart Rate / physiology
  • Humans
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism
  • Microtubule-Associated Proteins / genetics
  • Microtubule-Associated Proteins / metabolism
  • Mitochondria / genetics*
  • Mitochondria / metabolism
  • Mitochondria / pathology
  • Mitochondrial Dynamics / genetics*
  • Mitochondrial Membrane Transport Proteins / genetics*
  • Mitochondrial Membrane Transport Proteins / metabolism
  • Mitochondrial Proteins / genetics*
  • Mitochondrial Proteins / metabolism
  • Mitophagy / genetics
  • Myocytes, Cardiac / metabolism
  • Myocytes, Cardiac / pathology
  • Peptide Elongation Factors / genetics
  • Peptide Elongation Factors / metabolism
  • Protein Kinases / genetics
  • Protein Kinases / metabolism
  • RNA, Messenger / genetics*
  • RNA, Messenger / metabolism


  • FIS1 protein, human
  • MIEF1 protein, human
  • MIEF2 protein, human
  • Membrane Proteins
  • Mff protein, human
  • Microtubule-Associated Proteins
  • Mitochondrial Membrane Transport Proteins
  • Mitochondrial Proteins
  • Peptide Elongation Factors
  • RNA, Messenger
  • Protein Kinases
  • PTEN-induced putative kinase
  • GTP Phosphohydrolases
  • MFN2 protein, human
  • Mfn1 protein, human
  • DNM1L protein, human
  • Dynamins

Supplementary concepts

  • Cardiomyopathy, Dilated, 1o