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Published on: June 14, 2016
The Role of Signalling Pathways in Myocardial Fibrosis in Hypertrophic Cardiomyopathy
Patryk Skórka1, Jakub Piotrowski1, Estera Bakinowska1
1Department of Physiology, Pomeranian Medical University, 70-111 Szczecin, Poland.
Insights
Hypertrophic cardiomyopathy (HCM), a genetic heart condition, involves cardiac fibrosis driven by cell interactions and signaling pathways. Monitoring pro-fibrotic molecules may help predict patient outcomes.
Area of Science:
- Cardiovascular Medicine
- Genetics
- Cell Biology
Background:
- Hypertrophic cardiomyopathy (HCM) is the most common inherited heart disease, characterized by left ventricular hypertrophy and fibrosis.
- Cardiac fibroblasts, myofibroblasts, and their interactions with cardiomyocytes and immune cells are key drivers of fibrosis progression in HCM.
- The complex pathogenesis of HCM involves multiple signaling pathways, with transforming growth factor-beta and angiotensin II being frequently studied.
Purpose of the Study:
- To review current evidence on the role of signaling pathways in the pathogenesis of hypertrophic cardiomyopathy.
- To explore the potential of monitoring pro-fibrotic molecules for predicting clinical outcomes in HCM patients.
Main Methods:
- Literature review of current evidence on signaling pathways in HCM pathogenesis.
- Discussion of the role of pro-fibrotic molecules in HCM progression and clinical outcomes.
Main Results:
- Signaling pathways, including TGF-β and Angiotensin II, are critically involved in cardiac fibrosis development in HCM.
- Cellular interactions between fibroblasts, cardiomyocytes, and immune cells significantly contribute to fibrosis progression.
- Pro-fibrotic molecules show potential as biomarkers for predicting clinical outcomes in HCM.
Conclusions:
- Understanding the intricate signaling pathways and cellular interactions is crucial for elucidating HCM pathogenesis.
- Monitoring pro-fibrotic molecules may offer a novel strategy for risk stratification and outcome prediction in hypertrophic cardiomyopathy patients.
Abstract:
Hypertrophic cardiomyopathy (HCM) is the most prevalent hereditary cardiovascular disorder, characterised by left ventricular hypertrophy and cardiac fibrosis. Cardiac fibroblasts, transformed into myofibroblasts, play a crucial role in the development of fibrosis. However, interactions between fibroblasts, cardiomyocytes, and immune cells are considered major mechanisms driving fibrosis progression. While the disease has a strong genetic background, its pathogenetic mechanisms remain complex and not fully understood. Several signalling pathways are implicated in fibrosis development. Among these, transforming growth factor-beta and angiotensin II are frequently studied in the context of cardiac fibrosis. In this review, we summarise the most current evidence on the involvement of signalling pathways in the pathogenesis of HCM. Additionally, we discuss the potential role of monitoring pro-fibrotic molecules in predicting clinical outcomes in patients with HCM.
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