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Introduction
Hypertension, also known as arterial hypertension, is a chronic medical condition in which the blood pressure in the arteries is elevated (1). Hypertension is classified as either primary or secondary hypertension, and primary hypertension accounts for approximately 90–95% of cases (2). In primary hypertension, the cause of the hypertensioin is not clearly defined, whereas in secondary hyptertension, the cause of the high blood pressure is clearly determined. Hypertension can lead to cardiac hypertrophy, aortic dissection and heart failure, due to structural changes in blood vessel walls and in the heart muscle, which has become a major burden to healthcare systems (3). Thus, hypertension is the leading risk factor for cardiovascular disease (4). According to a report of the World Health Organization in 2011, cardiovascular diseases are the leading cause of morbidity and mortality worldwide (5).
As a multifactorial disease, hypertension results from a complex interaction of environmental factors and genetic factors (6). Numerous common genetic variants, as well as some rare genetic variants have been identified to affact blood pressure (7,8). For instance, bone morphogenetic protein receptor type 2, which belongs to the transforming growth factor (TGF)-β superfamily of receptors, has been found to be mutated in the majority of cases of hypertension (9). Interleukin (IL)-17 has also been thought to be involved in hypertension due to its role in increasing the production of some other immune system chemical signals, such as IL-1, IL-6 and tumor necrosis factor (TNF)-α (10). Additionally, Austin et al (11) suggested that mutations in caveolin-1 are associated with pulmonary arterial hypertension. Despite advances in understanding the etiology of hypertension, the genetic basis responsible for this disease remains poorly elucidated.
Presently, there are many species of animals used as models of hypertension. In our study, the microarray dataset, GSE54015, which contained data from Schlager BPH/2J and BPN/3J mouse models was downloaded for analysis. of note, Puig et al (12) also used the same mouse models to identify potential pharmacological targets of hypertension. In this study, we identified the differentially expressed genes (DEGs) between normotensive mice and hypertensive mice of both genders. Additionally, we performed functional enrichment analyses and protein-protein interaction (PPI) networks analysis to study and identify the pathways and DEGs associated with hypertension. Furthermore, transcription factors (TFs) and...