Comorbidity of Anxiety and Hypertension: Common Risk Factors and Potential Mechanisms.

Anxiety is more common in patients with hypertension, and these two conditions frequently coexist. Recently, more emphasis has been placed on determining etiology in patients with comorbid hypertension and anxiety. This review focuses on the common risk factors and potential mechanisms of comorbid hypertension and anxiety. Firstly, we analyze the common risk factors of comorbid hypertension and anxiety including age, smoking, alcohol abuse, obesity, lead, and traffic noise. The specific mechanisms underlying hypertension and anxiety were subsequently discussed, including interleukin (IL)-6 (IL-6), IL-17, reactive oxygen species (ROS), and gut dysbiosis. Increased IL-6, IL-17, and ROS accelerate the development of hypertension and anxiety. Gut dysbiosis leads to hypertension and anxiety by reducing short-chain fatty acids, vitamin D, and 5-hydroxytryptamine (5-HT), and increasing trimethylamine N-oxide (TAMO) and MYC. These shared risk factors and potential mechanisms may provide an effective strategy for treating and preventing hypertension and comorbid anxiety.

MiRNA-200a induce cell apoptosis in renal cell carcinoma by directly targeting SIRT1.

Accumulating evidence indicates that microRNAs are implicated in tumor initiation and progression through negatively regulating oncogenes or tumor suppressor genes. In the present study, we report that the expression of miR-200a was significantly lower in renal cell carcinoma (RCC) specimens and RCC cell lines. Restoration of miR-200a suppressed cell growth, arrested cell cycle progression, and promoted cell apoptosis in RCC cell lines. We next used qRT-PCR array technology to identify Sirtuin 1 (SIRT1) as one of the downregulated proteins during miR-200a overexpression in 786-O cells. Following a further assay by luciferase reporter system, SIRT1 was validated as a direct target of miR-200a. Moreover, siRNA-mediated knockdown of SIRT1 could partially phenocopy the effects of miR-200a overexpression. In contrast, overexpression of truncated SIRT1 (without an endogenous 3'-UTR) could rescue the effect of miR-200a overexpression on 786-O cells, which suggested that SIRT1 3'-UTR is targeted by miR-200a specifically. These observations provide further evidence for a critical tumor-suppressive role of the miR-200a in RCC in addition to identifying a novel regulatory mechanism, which may contribute to SIRT1 upregulation in RCC.