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Systems Network Genomic Analysis Reveals Cardioprotective Effect of MURC/Cavin-4 Deletion Against

Masahiro Nishi1, Takehiro Ogata1,2, Carlo Vittorio Cannistraci3,4

  • 1Department of Cardiovascular Medicine Graduate School of Medical Science Kyoto Prefectural University of Medicine Kyoto Japan.

Journal of the American Heart Association
|August 1, 2019
PubMed

Insights

Muscle-restricted coiled-coil protein (MURC) deletion protects against heart ischemia/reperfusion injury by reducing reactive oxygen species and inhibiting apoptosis via STAT3 signaling. MURC inhibition may be a therapeutic strategy for heart attack recovery.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Systems Biology

Background:

  • Ischemia/reperfusion (I/R) injury is a major challenge in treating ischemic heart disease.
  • Muscle-restricted coiled-coil protein (MURC)/Cavin-4 is implicated in heart conditions but its role in I/R injury is unknown.

Purpose of the Study:

  • To investigate the role of MURC in cardiac I/R injury.
  • To elucidate the molecular mechanisms underlying MURC's effect on I/R injury.

Main Methods:

  • Systems network genomic analysis (PC-corr network inference) on microarray data.
  • Experimental validation using I/R-injured mouse hearts and isolated cardiomyocytes.
  • Inhibition of STAT3 signaling pathway.

Main Results:

  • MURC deletion reduced infarct size and improved heart function in I/R-injured mice.
  • MURC deficiency suppressed reactive oxygen species-related genes (EGR1, DDIT4) and modulated apoptosis pathways (STAT3, BCL2, caspase 3).
  • STAT3 inhibition abrogated the cardioprotective effects of MURC deletion.

Conclusions:

  • MURC modulates cardiac I/R injury by regulating reactive oxygen species-induced cell death.
  • MURC plays a role in STAT3-mediated anti-apoptosis in the heart.
  • Functional inhibition of MURC shows potential for treating cardiac I/R injury.
Keywords:
apoptosiscaveolaeischemia reperfusion injuryreactive oxygen speciessystems biology

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