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Molecular mechanisms behind progressing chronic inflammatory dilated cardiomyopathy

Daiva Bironaite1, Dainius Daunoravicius2, Julius Bogomolovas3

  • 1Dept. of Stem Cell Biology, State Research Institute, Center for Innovative Medicine, Zygimantu 9, LT01102, Vilnius, Lithuania. d.bironaite@imcentras.lt.

BMC Cardiovascular Disorders
|April 19, 2015
PubMed

Insights

Inflammatory dilated cardiomyopathy (iDCM) involves elevated IL-6 and caspase levels, indicating mitochondrial involvement in cardiomyocyte apoptosis. Targeting inflammation and apoptosis may improve iDCM therapy before heart failure develops.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Immunology

Background:

  • Inflammatory dilated cardiomyopathy (iDCM) is a serious condition leading to heart failure and potential heart transplantation.
  • Understanding the molecular mechanisms of iDCM is crucial for developing effective therapeutic interventions.

Purpose of the Study:

  • To evaluate sera and biopsy samples from chronic iDCM patients.
  • To investigate molecular mechanisms underlying left ventricular remodeling and disease progression in iDCM.

Main Methods:

  • Patients were classified into inflammatory and non-inflammatory DCM groups based on immunohistochemical markers (CD3, CD45Ro, CD68).
  • Inflammation, apoptosis, necrosis, and fibrosis were assessed using ELISA, chemiluminescent, immunohistochemical, and histological assays.

Main Results:

  • Elevated serum IL-6, caspase-9, -8, and -3 levels were observed in iDCM patients.
  • Increased Hsp60 release suggested mitochondrial involvement in cardiomyocyte apoptosis.
  • Upregulation of MMP9/TIMP1 in biopsies correlated with apoptosis and ECM degradation, indicating a role in cell death initiation.

Conclusions:

  • Increased serum IL-6, MMP9/TIMP1, and caspases reflect molecular mechanisms in chronic iDCM myocardium.
  • Intramyocardial inflammation activates apoptotic pathways, potentially linked to the extrinsic pathway via Bax.
  • Chronic iDCM is characterized by intrinsic myocardial apoptosis, absence of necrosis, and reduced fibrosis, suggesting combined anti-inflammatory and anti-apoptotic treatments.
Abstract

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