Effects of blood pressure goals on cardiovascular outcomes in hypertensive patients.

INTRODUCTION: The aim of the study was to evaluate the effects of blood pressure (BP) goals on cardiovascular outcomes in hypertensive patients. MATERIAL AND METHODS: Primary hypertensive patients were retrospectively enrolled from outpatient clinics. The demographics, comorbidities, laboratory parameters and glomerular filtration rate (GFR) were collected. All participants were followed for 1 year. Cardiovascular outcomes included composite of all-cause mortality, non-fatal myocardial infarction, and non-fatal ischemic stroke/transient ischemic attack. Adverse event was defined as falling down and GFR decrease at follow-up. RESULTS: A total of 1226 patients were included. Based on therapeutic BP goals, participants were divided into low (< 130/80 mm Hg) and high (< 140/90 mm Hg) therapeutic goal groups and an uncontrolled hypertension (≥ 140/90 mm Hg) group. Compared to the low therapeutic goal group, patients in the uncontrolled group were older and more likely to be smokers, have longer duration of hypertension, diabetes mellitus, lower GFR and higher prevalent ischemic stroke (p < 0.05). Patients in the uncontrolled hypertension group had higher incidence of composite endpoints than low and high therapeutic goal groups. Two cases of falling down were observed in the low therapeutic goal group and no significant changes in GFR were observed. With adjustment for confounding factors, the uncontrolled hypertension group had higher risk of composite endpoints compared to low and high therapeutic goal groups, and these benefits were more prominent in the low versus high therapeutic goal group. CONCLUSIONS: In hypertension patients, when compared to uncontrolled hypertension patients, low therapeutic BP goal is associated with better cardiovascular outcomes than high therapeutic BP goal.

microRNA-206 overexpression inhibits epithelial-mesenchymal transition and glomerulosclerosis in rats with chronic kidney disease by inhibiting JAK/STAT signaling pathway.

Chronic kidney disease (CKD) is a traumatic disease with significant psychic consequences to the patient's overall physical condition. microRNA-206 (miR-206) has been reported to play an essential role in the development of various diseases. The purpose of the present study is to investigate the effect of miR-206 through the JAK/STAT signaling pathway on epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells and glomerulosclerosis in rats with CKD. The targeting relationship between miR-206 and ANXA1 was verified. To explore the role of miR-206 in CKD, the model of CKD rats was established to detect glomerular sclerosis index (GSI), contents of interleukin-6 (IL-6) and transforming growth factor-beta1 (TGF-ß1), and expression of type IV collagen. Moreover, to further determine the roles of both miR-206 and the JAK/STAT signaling pathway in CKD, the gain- and loss-of function approaches were performed with the expression of ANXA1, α-SMA, E-cadherin, vimentin, N-cadherin, and the JAK/STAT signaling pathway-related genes detected. miR-206 negatively targeted ANXA1. Overexpressed miR-206 inhibited the degeneration and interstitial fibrosis of renal tubular epithelial cells, decreased GSI of rats, and the expression of type IV collagen, TGF-ß1 and IL-6. Overexpressed miR-206 inhibited the degeneration of renal tubular epithelial cells, the expression of ANXA1, α-SMA, TGF-ß1, p-STAT3, STAT3, p-STAT1, STAT1, p-JAK2, and JAK2, while promoted the expression of E-cadherin. Taken together the results, miR-206 inhibits EMT of renal tubular epithelial cells and glomerulosclerosis by inactivating the JAK/STAT signaling pathway via ANXA1 in CKD.