BackgroundHypertension is a leading global health threat and a major cardiovascular disease. Since clinical interventions are effective in delaying the disease progression from prehypertension to hypertension, diagnostic prediction models to identify patient populations at high risk for hypertension are imperative.MethodsBoth PubMed and Embase databases were searched for eligible reports of either prediction models or risk scores of hypertension. The study data were collected, including risk factors, statistic methods, characteristics of study design and participants, performance measurement, etc.ResultsFrom the searched literature, 26 studies reporting 48 prediction models were selected. Among them, 20 reports studied the established models using traditional risk factors, such as body mass index (BMI), age, smoking, blood pressure (BP) level, parental history of hypertension, and biochemical factors, whereas 6 reports used genetic risk score (GRS) as the prediction factor. AUC ranged from 0.64 to 0.97, and C-statistic ranged from 60% to 90%.ConclusionsThe traditional models are still the predominant risk prediction models for hypertension, but recently, more models have begun to incorporate genetic factors as part of their model predictors. However, these genetic predictors need to be well selected. The current reported models have acceptable to good discrimination and calibration ability, but whether the models can be applied in clinical practice still needs more validation and adjustment.

Mitofusin-2 (MFN2) is a mitochondrial protein associated with mitochondrial fusion process. It was initially identified as a hyperplasia suppressor and implicated in Charcot-Marie-Tooth disease. Recent studies showed that MFN2 played important roles in the development of multiple tumors. Here we examined MFN2 expression in 30 lung adenocarcinoma samples and revealed that the expression of MFN2 was significantly higher in lung adenocarcinoma tissues as compared to adjacent normal tissues. We then investigated the impact of MFN2 knockdown on A549 human lung adenocarcinoma cells and showed that cell proliferation, cell cycle and invasion behavior were all deregulated by MFN2 knockdown. And deregulation of cell cycle pathway after MFN2 knockdown was confirmed by microarray analysis. Furthermore, microarray analysis also revealed that different oncogenes such as RAP1A, RALB and ITGA2 were oppositely regulated by MFN2, which provided molecular clues for the paradoxical functions of MFN2 in tumor development. Taken together, our study unraveled the tumor-promoting functions of MFN2 in lung adenocarcinoma and implicated that the role of MFN2 in cancer development might be more complicated than expected and should be explored in detail in the future.

Hypertension, a multifactorial disease, is a major risk factor for the development of stroke, coronary artery disease, heart failure, and chronic renal failure. However, its underlying cellular and molecular mechanisms remain largely elusive. Numerous studies have shown that microRNAs (miRNAs) are involved in a variety of cellular processes, including cellular proliferation, apoptosis, differentiation, and the development of diseases. microRNA-21 (miR-21), a conserved single-stranded non-coding RNA that is composed of approximately 22 nucleotides, is one of the most intensively studied miRNAs in recent years, and it can regulate gene expression at the post-transcriptional level. miR-21 is expressed in many kinds of tumors and in the cardiovascular system, and it plays an important role in the occurrence and development of cardiovascular diseases. In recent years, more and more evidence indicates that miR-21 plays an important role in hypertension. This article reviews the source, function, and altered levels of miR-21 in hypertension and the role of miR-21 in the pathogenesis of hypertension and target organ damage (TOD). The potential role of miR-21 as a new target for predicting and treating hypertension is also explored.