Atorvastatin Prevents Myocardial Fibrosis in Spontaneous Hypertension via Interleukin-6 (IL-6)/Signal Transducer and Activator of Transcription 3 (STAT3)/Endothelin-1 (ET-1) Pathway.

BACKGROUND Hypertension is a leading global disease, and myocardial fibrosis is an important adverse effect of hypertension, seriously threatening human health. The IL-6/STAT3 pathway and endothelin-1 (ET-1) were previously suggested to play a part in myocardial fibrosis. MATERIAL AND METHODS To investigate the role of Atorvastatin (Ato) in spontaneous hypertension, systolic blood pressure (SBP) and left ventricular mass index (LVMI) were measured, and Masson trichrome staining was performed.

Loss of AMIGO2 causes dramatic damage to cardiac preservation after ischemic injury.

Background: Recent studies have identified amphoterin-induced gene and open reading frame (AMIGO2). The role of AMIGO2 in tumour research is well-studied, but its role in ischemic heart diseases is seldom reported. In the present study, the role of AMIGO2 in myocardial infarction (MI) is under investigation for the first time.

TIEG1 deficiency confers enhanced myocardial protection in the infarcted heart by mediating the Pten/Akt signalling pathway.

The transforming growth factor (TGF)-β-inducible early gene-1 (TIEG1) plays a crucial role in modulating cell apoptosis and proliferation in a number of diseases, including pancreatic cancer, leukaemia and osteoporosis. However, the functional role of TIEG1 in the heart has not been fully defined. In this study, we first investigated the role of TIEG1 in ischaemic heart disease.