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24 \ 02 \ 2020

How do TGFβ1 and HGF regulate CTGF expression in human atrial fibroblasts?

Lenka Sonnkova                


Heart disease is responsible for the most deaths worldwide for both men and women of all races. The term “heart disease”, includes different types of disease such as coronary artery disease (CAD), heart attack, congestive heart failure, and congenital heart disease.

One of the most common cardiovascular diseases is atrial fibrillation (AF), with an occurrence of 1% in the general population. It is characterized by rapid, chaotic and irregular beating of the heart's two upper chambers (the atria).

Atrial fibrillation symptoms often include heart palpitations, shortness of breath and weakness. The disease is associated with an increased risk of heart failure, dementia, and stroke

Factors that increase the risk of AF include: obesity, excess alcohol intake, tobacco smoking, diabetes mellitus, sleep apnea etc.

A common feature of clinical atrial fibrillation is myocardial fibrosis (MF). This disease is characterized by net accumulation of extracellular matrix in the myocardium. A variety of hemodynamic, toxic, metabolic, and immunologic disturbances trigger fibrotic remodelling of the myocardium. Myocardial fibrosis is a significant global health problem associated with nearly all forms of heart disease and is a predictive factor for sudden cardiac death.

It is known that myocardial fibrosis progression is controlled by various factors, e.g. renin‐angiotensin‐aldosterone system, chemokines, cytokines and growth factors.


Chen and his team from Provincial Clinical Medicine College of Fujian Medical University in Fuzhou conducted the study to investigate the mechanism of interaction among transforming growth factor‐β1 (TGFβ1), hepatocyte growth factor (HGF) and connective tissue growth factor (CTGF) in atrial fibrosis regulation, and the relationship between atrial fibrosis and atrial fibrillation. 

Twenty patients with rheumatic heart disease who underwent valve replacement surgery in Fujian Provincial Hospital were enrolled. Patients were divided into sinus rhythm (SR) and chronic atrial fibrillation (CAF) groups, with 10 patients in each group.

It was found that reciprocal equilibrium of TGF β1 and HGF regulates organ fibrosis. TGFβ1increases the activity and expression of the CTGF promoter in cardiac fibroblasts. CTGF activates pro‐fibrotic signalling pathways and its overexpression is associated with atrial fibrosis in patients with chronic atrial fibrillation. On the other hand, HGF is an anti‐fibrotic factor for the heart and significantly reduces TGFβ1‐induced CTGF production in fibroblasts. 

The Following picture shows is comparative histograms of CTGF protein expression detected by immunofluorescence in each experimental group (n = 10).


The results demonstrated that TGF β1, HGF, and CTGF together play a role in atrial remodelling and arrhythmias induced by atrial fibrosis and have potential as therapeutic targets for the treatment of these fibrotic diseases. 

Based on the research thus far, TGF β1 and CTGF antibodies and human recombinant HGF warrant further investigation for the treatment of atrial fibrosis. 

Sources: J Cell Mol Med., DOI: 10.1111/jcmm.14165
JACC, DOI: 10.1016/j.jacc.2010.11.013

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