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Fibrosis markers and CRIM1 increase in chronic heart failure of increasing severity
Ermanno Eleuteri1, Antonino Di Stefano, Davide Vallese
1Divisione di Cardiologia Riabilitativa e Laboratorio di Citoimmunopatologia Apparato Cardio-Respiratorio, Fondazione Salvatore Maugeri , IRCCS, Veruno, NO , Italy .
Insights
In chronic heart failure (CHF), serum levels of procollagen type III (PIPIII) and the BMPs inhibitor CRIM1 are elevated. This suggests a pro-fibrotic imbalance, highlighting potential therapeutic targets for heart failure.
Area of Science:
- Cardiology
- Biochemistry
- Molecular Biology
Background:
- Chronic heart failure (CHF) involves complex mechanisms including fibrosis.
- Identifying regulators of fibrosis is crucial for understanding CHF progression.
Purpose of the Study:
- To quantify serum levels of key fibrosis regulators in patients with CHF.
- To investigate the relationship between these regulators and disease severity.
Main Methods:
- Enzyme-linked immunosorbent assays (ELISA) were employed.
- Serum samples from 66 CHF patients (NYHA classes I-III) and 14 controls were analyzed.
- Quantified markers included procollagen type I and III (PIPI and PIPIII), collagen I and III, BMPs (1, 2, 3, 7), SDF1α, CXCR4, fibulin family, BMPER, CRIM1, and BAMBI.
Main Results:
- Elevated serum levels of PIPIII, SDF1α, and CRIM1 were observed in CHF patients compared to controls.
- CRIM1 levels showed a positive correlation with PIPIII levels.
- TGFβR2 and CRIM1 were also found to be increased in CHF.
Conclusions:
- The study identified an increase in PIPIII and CRIM1 in CHF patients.
- The correlation between PIPIII and CRIM1 suggests an imbalance favoring pro-fibrotic processes.
- CRIM1, an inhibitor of Bone Morphogenetic Proteins (BMPs), may play a significant role in CHF-associated fibrosis.
Background:
Fibrosis suppressors/activators in chronic heart failure (CHF) is a topic of investigation.
Aim:
To quantify serum levels of fibrosis regulators in CHF.
Methods:
ELISA tests were used to quantify fibrosis regulators, procollagen type-(PIP)I, (PIP)III, collagen-I, III, BMP1,2,3,7, SDF1α, CXCR4, fibulin 1,2,3, BMPER, CRIM1 and BAMBI in 66 CHF (NYHA class I, n = 9; II, n = 34; III n = 23), and in 14 controls.
Results:
In CHF, TGFβR2, PIPIII, SDF1α and CRIM1 were increased. PIPIII correlated with CRIM1.
Conclusions:
The BMPs inhibitor CRIM1 is increased and correlates with higher levels of serum PIPIII showing an imbalance in favor of pro-fibrotic mechanisms in CHF.
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