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Desmin Correlated with Cx43 May Facilitate Intercellular Electrical Coupling during Chronic Heart Failure

Junxian Cao1, Qianping Gao1, Hongyan Chen2

  • 1Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China.

Evidence-Based Complementary and Alternative Medicine : Ecam
|July 21, 2021
PubMed

Insights

Reduced desmin protein in heart failure impairs cardiomyocyte function. This study reveals desmin

Area of Science:

  • Cardiology
  • Cell Biology
  • Biochemistry

Background:

  • Desmin is a key intermediate filament protein in cardiomyocytes, crucial for muscle health.
  • Reduced desmin levels in cardiomyocytes are linked to poor heart failure prognosis and contractile dysfunction.
  • The precise mechanisms underlying desmin's role in heart failure remain unclear.

Purpose of the Study:

  • To investigate the expression levels of desmin in human and rat heart failure models.
  • To explore the association between desmin and gap junction proteins connexin 43 (Cx43) and zonula occludens-1 (ZO-1).
  • To evaluate the potential of desmin as a therapeutic target for heart failure.

Main Methods:

  • Western blotting and qPCR to measure desmin expression in failing hearts and cardiomyocytes.
  • Immunoprecipitation assays to determine the association between desmin and Cx43.
  • Co-culture experiments to assess the electrical coupling of skeletal myoblasts with cardiac myocytes in the presence of desmin.

Main Results:

  • Desmin protein levels were significantly reduced in failed human and rat hearts and isolated cardiomyocytes.
  • Desmin was found to associate with Cx43 in cardiomyocytes.
  • Desmin overexpression in skeletal myoblasts enhanced their electrical coupling with cardiac myocytes by influencing Cx43 and ZO-1 expression and complex formation.

Conclusions:

  • Desmin deficiency contributes to myocyte dysfunction in heart failure.
  • Desmin interacts with Cx43 and ZO-1, enhancing cell-to-cell electrical coupling.
  • Preserving or restoring desmin levels may offer a novel therapeutic strategy for attenuating heart failure.

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