Transforming growth factor beta (TGF-β) mediates cardiac fibrosis and induces diabetic cardiomyopathy
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Yiyang Yue1, Ke Meng2, Yuejie Pu2
1College of Agriculture & Biotechnology, Zhejiang University, China.
Insights
Diabetic cardiomyopathy involves cardiac fibrosis, leading to heart failure. Understanding transforming growth factor beta (TGF-β) pathways is key to managing this diabetic complication.
Area of Science:
- Cardiology
- Endocrinology
- Molecular Biology
Background:
- Cardiovascular diseases are a major cause of death in diabetic patients.
- Diabetic cardiomyopathy (DCM) leads to heart failure, with cardiac fibrosis playing a key role.
- Mechanisms of DCM pathogenesis, including left ventricular hypertrophy and dysfunction, are not fully understood.
Purpose of the Study:
- To review molecular pathways activating transforming growth factor beta (TGF-β).
- To elucidate the role of TGF-β in diabetes-induced cardiac fibrosis and DCM.
- To propose potential management strategies for DCM by illustrating TGF-β pathways.
Main Methods:
- Literature review of molecular mechanisms in diabetic cardiomyopathy.
- Analysis of studies on microRNAs, long non-coding RNAs, and TGF-β signaling in diabetes.
- Examination of SMAD-dependent and independent pathways in fibrogenesis.
Main Results:
- Hyperglycemia in diabetes alters expression of miRNAs, lncRNAs, and TGF-β pathway components.
- Activated TGF-β promotes cardiac fibrosis, contributing to DCM.
- Fibrosis leads to pathological changes including left ventricular hypertrophy and diastolic/systolic dysfunction.
Conclusions:
- TGF-β signaling is a critical mediator in the development of diabetic cardiomyopathy.
- Understanding TGF-β activation pathways offers therapeutic targets for DCM.
- Targeting fibrogenesis may provide an efficient management strategy for diabetic heart disease.
Abstract:
Cardiovascular diseases account for the major cause of morbidity and mortality among individuals with diabetes. The diabetic cardiomyopathy (DCM) is a type of diabetic cardiovascular disease, which further directs to the heart failure. The researchers found that diabetes induced cardiac fibrosis plays a vital role in several of the pathological changes that associated with DCM, causing left ventricular hypertrophy (LVH), diastolic dysfunction and systolic dysfunction. However, the mechanisms involved in the pathogenesis of DCM are still elusive. Many studies have demonstrated that the transforming growth factor beta (TGF-β) is one of the molecular mediators implicated in the progression of fibrogenesis. In diabetes, hyperglycemia causes the expression changes of microRNAs (miRNAs), long non-coding RNAs (lncRNAs), TGF-β genes, TGF-β proteins and their receptors. Activated TGF-β further leads to cardiac fibrosis, which in turn inducing DCM through the SMAD-dependent and independent pathways. Here, we reviewed the the molecular pathways that activate TGF-β then leading to cardiac fibrosis, which induced the pathological changes of DCM. Illustrating the pathways of TGF-ß would propose an efficient way for the management of diabetic cardiomyopathy (see Fig. 1).