Related Experiment Video
Updated: May 7, 2026

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
Published on: June 14, 2016
Fibrosis in heart failure subtypes
G Toprak1, H Yüksel, Ö Demirpençe
1Medical Biochemistry, Dicle University, Diyarbakir, Turkey. oevliya@hotmail.com.
Insights
Biomarker levels differ between dilated and ischemic cardiomyopathy. Matrix metalloproteinases (MMPs) and Galectin-3 are key in cardiac remodeling, with prolidase potentially involved in heart failure fibrosis.
Area of Science:
- Cardiology
- Biochemistry
- Biomarker Research
Background:
- Dilated cardiomyopathy (HF-D) and ischemic cardiomyopathy (HF-I) present distinct pathophysiological profiles.
- Understanding biomarker differences is crucial for diagnosing and managing heart failure subtypes.
- Extracellular matrix (ECM) turnover, inflammation, and oxidative stress are implicated in heart failure progression.
Purpose of the Study:
- To compare biomarker concentrations between HF-D and HF-I patients.
- To investigate correlations of biomarkers related to inflammation, ECM turnover, and oxidative stress.
- To elucidate the roles of specific biomarkers in different heart failure etiologies.
Main Methods:
- The study included 36 HF-D patients, 44 HF-I patients, and 38 controls.
- Measurements included matrix metalloproteinases (MMP-1, MMP-2, MMP-9, MMP-13), Galectin-3, prolidase, TNF-alpha, and oxidative stress index (OSI).
- Statistical analyses compared biomarker concentrations and correlations between groups.
Main Results:
- Serum levels of MMP-2, MMP-9, and prolidase were elevated in HF-I compared to controls, with stronger significance in HF-D.
- TNF-alpha and OSI were increased in heart failure patients generally, without significant differences between HF-D and HF-I.
- Galectin-3 was significantly higher in HF-D compared to HF-I, and MMP-9 correlated positively with prolidase activity.
Conclusions:
- Matrix metalloproteinases (MMPs) and Galectin-3 play significant roles in cardiac remodeling.
- Prolidase may have an uncharacterized role in heart failure fibrosis.
- These findings highlight distinct biomarker profiles that may aid in differentiating heart failure etiologies and understanding disease mechanisms.
Background:
The differences in concentrations of biomarkers between heart failure patients with dilated cardiomyopathy (HF-D) and with ischemic cardiomyopathy (HF-I) have yet to be defined. The objectives of this study were to compare the concentrations and correlation of biomarkers of inflammation, extracellular matrix (ECM) turnover and oxidative stress parameters between these populations.
Patients And Methods:
Our study consisted of 36 subjects with HF-D (LVSD = 47.2 ± 7.3 mm, LVDD = 65.1 ± 6.3 mm), 44 subjects with HF-I (LVSD = 38.0 ± 4.4 mm, LVDD = 58.5 ± 6.0 mm) and 38 controls without heart failure. Concentrations of matrix metalloproteinase (MMP)-1, MMP-2, MMP-9, MMP-13, Galectin-3, prolidase, TNF-alpha, and oxidative stress index (OSI) were measured.
Results:
Serum levels of MMP-2, MMP-9, and prolidase were significantly increased in HF-I group compared to healthy controls (p = 0.039, 0.019, 0.012 respectively), whereas the increases in MMP-1 and MMP-13 were not significant. This significance was stronger in the HF-D group than the HF-I group (p = 0.004, 0.001, 0.002 respectively). TNF-α, a marker of inflammation, was significantly increased in heart failure (p = 0.004) but there was no difference between HF-D and HF-I groups; however, Galectin-3 was significantly increased in the HF-D group compared to the HF-I group (p = 0.005). OSI showed the same response pattern as TNF-α (p = 0.019, 0.002 respectively). There was a positive correlation of MMP-9 levels with prolidase activity (r = 0.612, p: 0.003).
Conclusions:
MMPs and Galectin-3 are important in cardiac remodeling; prolidase may share an undefined role in fibrosis in heart failure and may have a role in the diffuse fibrosis of heart failure.
Related Concept Videos
Pathophysiology of Heart Failure
Heart Failure IV: Classification and Diagnostic Evaluation
Heart Failure II: Pathophysiology
Heart Failure I: Introduction
Heart Failure III: Clinical Manifestations
Heart Failure V: Medical Management
