Myocardial remodeling is a common pathological physiology change for a variety of heart diseases under stimulation such as stress or ischemia. The engine body will release a lot of cytokines to promote the change of myocardial structure and ultimately lead to heart failure. Myocardial remodeling includes myocardial cells remodeling and the extracellular matrix remodeling. In recent years, we find that the function of adipose tissue is not only about energy storage, buffering to protect, supporting and filling, but also has a powerful function of secretion. Adipose tissue can secrete various adipocytokines, such as leptin, adiponectin, visfatin, omentin, angiotensin Ⅱ, and so on. Current studies have shown that adipocytokines and myocardial remodeling are intimated. And this article will summarize the function of adipocytokines on myocardial remodeling.
Congestive pulmonary arterial hypertension (PAH) is one of the most common complications of left to right shunt congenital heart disease. With the pulmonary artery pressure increasing, the shunt direction will reverse, eventually develop into Eisenmenger syndrome, and affect the patients' life. Studies in recent years have found that angiotensin -(1-7) and brain natriuretic peptide can adversely affect renin-angiotensin aldosterone system (RAAS), stromal cell derived factor can delay the pulmonary vascular remodeling, von Willebrand factor marks the pulmonary vascular endothelial function impaired, microRNA causes damage and homocysteine play a protective role in pulmonary vascular endothelial function. The RAAS activation, pulmonary vascular remodeling and endothelial dysfunction are related to the formation and development of PAH. We produced a comprehensive literature review about serological indexes in congestive PAH in this review.