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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
Summary
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.
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