RESUMEN
OBJECTIVE: This study systematically evaluated the effects of Tai Chi exercise on blood pressure, body mass index (BMI), and quality of life (QOL) in patients with hypertension. A meta-analysis was performed to provide a reliable reference for clinical practice. METHODS: We searched for randomized controlled trials (RCTs) in five English databases and two Chinese databases, with the earliest data dated December 5, 2020. A quality assessment of the methods and a meta-analysis were also conducted. RESULTS: The meta-analysis of 24 studies showed that the intervention group showed better outcomes in terms of systolic blood pressure (SBP) (SMD -1.05, 95% CI -1.44 to -0.67, P ≤ 0.001; I 2 = 93.7%), diastolic blood pressure (DBP) (SMD -0.91, 95% CI -1.24 to -0.58, P ≤ 0.001; I 2 = 91.9%), and QOL (physical functioning (SMD 0.86, 95% CI 0.36 to 1.37, P=0.001; I 2 = 91.3%), role-physical (SMD 0.86, 95% CI 0.61 to 1.11, P ≤ 0.001; I 2 = 65%), general health (SMD 0.75, 95% CI 0.32 to 1.17, P=0.001; I 2 = 88.1%), bodily pain (SMD 0.65, 95% CI 0.29 to 1.00, P ≤ 0.001; I 2 = 83.1%), vitality (SMD 0.71, 95% CI 0.34 to 1.07, P ≤ 0.001; I 2 = 84.3%), social functioning (SMD 0.63, 95% CI 0.07 to 1.19, P=0.027; I 2 = 93.1%), role-emotional (SMD 0.64, 95% CI 0.22 to 1.06, P=0.003; I 2 = 88.1%), and mental health (SMD 0.73, 95% CI 0.31 to 1.16, P=0.001; I 2 = 88.2%)) compared to those of the control group. However, no significant improvements were seen in BMI of the intervention group (SMD -0.08, 95% CI -0.35 to -0.19, P=0.554; I 2 = 69.4%) compared to that of the control group. CONCLUSION: Tai Chi is an effective intervention to improve SBP and DBP in patients with essential hypertension.
RESUMEN
Previous studies have demonstrated that calcium-/calmodulin-dependent protein kinase II (CaMKII) and calcineurin A-nuclear factor of activated T-cell (CnA-NFAT) signaling pathways play key roles in cardiac hypertrophy (CH). However, the interaction between CaMKII and CnA-NFAT signaling remains unclear. H9c2 cells were cultured and treated with angiotensin II (Ang II) with or without silenced CaMKIIδ (siCaMKII) and cyclosporine A (CsA, a calcineurin inhibitor) and subsequently treated with Wenxin Keli (WXKL). Patch clamp recording was conducted to assess L-type Ca2+ current (ICa-L), and the expression of proteins involved in signaling pathways was measured by western blotting. Myocardial cytoskeletal protein and nuclear translocation of target proteins were assessed by immunofluorescence. The results indicated that siCaMKII suppressed Ang II-induced CH, as evidenced by reduced cell surface area and ICa-L. Notably, siCaMKII inhibited Ang II-induced activation of CnA and NFATc4 nuclear transfer. Inflammatory signaling was inhibited by siCaMKII and WXKL. Interestingly, CsA inhibited CnA-NFAT pathway expression but activated CaMKII signaling. In conclusion, siCaMKII may improve CH, possibly by blocking CnA-NFAT and MyD88 signaling, and WXKL has a similar effect. These data suggest that inhibiting CaMKII, but not CnA, may be a promising approach to attenuate CH and arrhythmia progression.