Signalling pathways, including transforming growth factor-beta and angiotensin II, drive myocardial fibrosis progression and may help predict clinical outcomes in hypertrophic cardiomyopathy.
This review highlights the role of signalling pathways like TGF-beta and angiotensin II in driving myocardial fibrosis in hypertrophic cardiomyopathy and discusses the potential of pro-fibrotic molecules as prognostic biomarkers.
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.
Skórka et al. (Fri,) conducted a review in Hypertrophic cardiomyopathy. Signalling pathways, including transforming growth factor-beta and angiotensin II, drive myocardial fibrosis progression and may help predict clinical outcomes in hypertrophic cardiomyopathy.