Effects of monitoring exercise rehabilitation with target intensity on the patient with twice PCI: A case report.

RATIONALE: As the core of cardiac rehabilitation (CR), early exercise rehabilitation is beneficial for patients with coronary heart disease (CHD), and center-based CR with target intensity is superior to home-based CR. However, there was no research to observe the effects of exercise rehabilitation on cardiopulmonary exercise capacity, oxygen uptake efficiency slope, endothelial function evaluated as flow-mediated vasodilation (FMD), and blood plasma lipoprotein-associated phospholipase A2 (Lp-PLA2) in CHD patients undergone percutaneous coronary intervention (PCI) for 3 months. PATIENT CONCERNS: A 57-year-old woman had been identified with triple vessel disease and undergone twice PCI for complete revascularization, however, there was no improvement in Lp-PLA2, FMD, and related indicators of cardiopulmonary exercise testing. DIAGNOSIS: Coronary angiography showed an 85% stenosis in the middle left anterior descending artery, an 85% stenosis in the proximity of a thick first-diagonal branch, a long 75 to 85% stenosis in the middle left circumflex artery, and a 90 to 95% stenosis in the proximal. The case was diagnosed as CHD. INTERVENTIONS: The patient obtained optimal medical therapy comprising therapeutic lifestyle changes, and began monitoring exercise rehabilitation with target intensity 3 months after the second PCI in the CR center. OUTCOMES: There were changes in cardiopulmonary exercise capacity, oxygen uptake efficiency slope, FMD, and Lp-PLA2 in the patient with 3 apparent stenotic coronary arteries who was done PCI twice, without or with postoperative exercise rehabilitation, respectively. LESSONS: We proved that monitoring exercise rehabilitation training with target intensity could improve the prognosis of chronic coronary syndrome patients, and it was never too late to do regular exercise rehabilitation.

The benefit of exercise rehabilitation guided by 6-minute walk test on lipoprotein-associated phospholipase A2 in patients with coronary heart disease undergoing percutaneous coronary intervention: a prospective randomized controlled study.

BACKGROUND: Lipoprotein-associated phospholipase A2 (Lp-PLA2) has been taken as a biomarker of inflammation in patients with acute coronary diseases. Regular exercise rehabilitation could attenuate inflammation and promote the rehabilitation of coronary heart disease (CHD). The level of Lp-PLA2 is negatively correlated with 6-min walk test (6-MWT). The exercise prescription of appropriate intensity is the basis of exercise rehabilitation. 6-MWT is associated with maximal oxygen consumption, and can be used to determine the intensity of exercise prescription guiding patients how to do exercise rehabilitation. The aim of this study was to observe the benefit of 6-MWT guided exercise rehabilitation on the level of Lp-PLA2 in patients with CHD undergoing percutaneous coronary intervention (PCI). METHODS: We prospectively, consecutively enrolled 100 patients between Dec 2018 and Dec 2020 in the fourth ward of the Department of Cardiology, Yuebei People's Hospital Affiliated to Shantou University. Eligible patients were 1:1 divided into Group A, with no exercise rehabilitation, and Group B, with regular exercise rehabilitation, using random number table method of simple randomization allocation. Clinical data such as general information, the profile of lipids and the level of Lp-PLA2 were collected at baseline and at 12-week follow-up. RESULTS: There were no statistically significant differences of the percentages of gender, hypertension, type-2 diabetes mellitus (T2DM), the profile of lipids and level of Lp-PLA2 between the groups at baseline (P > 0.05). The level of Lp-PLA2 decreased at 12-week follow-up, moreover, the decline of the Lp-PLA2 level in Group B was more significant than that in Group A (t = 2.875, P = 0.005). Multivariate linear regression analysis indicated that exercise rehabilitation was independently correlated with the level of Lp-PLA2 (ß' = - 0.258, t = - 2.542, P = 0.013). CONCLUSION: Exercise rehabilitation for 12 weeks guided by 6-MWT can further reduce the level of LP-PLA2 in patients with CHD undergoing PCI. Trial registration This trial was registered on the Chinese Clinical Trial Registry: ChiCTR2100048124, registered 3 July 2021- Retrospectively registered. The study protocol adheres to the CONSORT guidelines.

PRMT7 promotes the growth of renal cell carcinoma through modulating the ß-catenin/C-MYC axis.

Arginine methylation is mainly catalyzed by protein arginine methyltransferases (PRMTs) and is one of the most common posttranslational modifications closely related to the development of cancer. PRMT7 is overexpressed in various tumors and promotes the malignant progression of tumors, but the expression and role of PRMT7 in renal cell carcinoma (RCC) remains unclear. Here, we report for the first time that the expression of PRMT7 is increased in clear cell renal cell carcinoma (ccRCC) tissues and that it may act as an independent predictor for the poor prognosis of ccRCC patients. We found that PRMT7 promotes RCC cell proliferation both in vitro and in vivo. Moreover, the methyltransferase inhibitor adenosine dialdehyde (Adox) blocks the action of PRMT7 in ccRCC cells. Furthermore, PRMT7 regulates the expression of C-MYC, which plays an important role in promoting ccRCC cell proliferation, and it accelerates the tumor development of RCC in a C-MYC-dependent manner. Mechanistically, PRMT7 upregulates the expression of C-MYC via methylating ß-catenin and inhibiting the ubiquitin-mediated degradation of ß-catenin. In conclusion, our study demonstrates that overexpressed PRMT7 in ccRCC cells acts as an oncogene to promote the growth of renal cell carcinoma through regulating the ß-catenin/C-MYC axis, thereby providing new strategies and targets for the treatment of ccRCC patients.

Sacubitril/Valsartan Reduces Fibrosis and Alleviates High-Salt Diet-Induced HFpEF in Rats.

Previous studies have confirmed the clinical efficacy of sacubitril/valsartan (Sac/Val) for the treatment of heart failure with reduced ejection fraction (HFrEF). However, the role of Sac/Val in heart failure with preserved ejection fraction (HFpEF) remains unclear. Sac/Val is a combination therapeutic medicine comprising sacubitril and valsartan that acts as a first angiotensin receptor blocker and neprilysin inhibitor (angiotensin-receptor neprilysin inhibitor (ARNI)). Here, we investigated the role of Sac/Val in high-salt diet-induced HFpEF coupled with vascular injury as well as the underlying mechanism. Rats were fed with high-salt feed, followed by intragastric administration of Sac/Val (68 mg/kg; i.g.). The results of functional tests revealed that a high-salt diet caused pathological injuries in the heart and vascular endothelium, which were significantly reversed by treatment with Sac/Val. Moreover, Sac/Val significantly decreased the levels of fibrotic factors, including type I collagen and type Ⅲ collagen, thus, reducing the ratio of MMP2/TIMP2 while increasing Smad7 levels. Further investigation suggested that Sac/Val probably reversed the effects of high-salt diet-induced HFpEF by inhibiting the activation of the TGF-ß1/Smad3 signaling pathway. Thus, treatment with Sac/Val effectively alleviated the symptoms of high-salt diet-induced HFpEF, probably by inhibiting fibrosis via the TGF-ß1/Smad3 signaling pathway, supporting the therapeutic potential of Sac/Val for the treatment of HFpEF.

Circular RNA circ-VANGL1 as a competing endogenous RNA contributes to bladder cancer progression by regulating miR-605-3p/VANGL1 pathway.

Increasing reports indicate that circular RNAs (circRNAs) are very important regulators in human diseases, including cancers. In bladder cancer (BC), several circRNAs have been reported to be involved in tumor progressions, such as circ-ITCH and circTCF25. However, the functions of most circRNAs in BC still remains largely unknown. In this study, we identified a novel circRNA termed as circ-VANGL1 by bioinformatics analysis. We found that circ-VANGL1 was highly expressed in BC tissues compared with adjacent normal tissues. Furthermore, we showed that circ-VANGL1 could serve as a prognostic marker for patients with BC. Through functional experiments, we found that circ-VANGL1 knockdown significantly suppressed BC cell proliferation, cell cycle, migration, and invasion in vitro. Besides, circ-VANGL1 silence inhibited BC cell propagation in vivo. Mechanistically, we identified circ-VANGL1 as a sponge of miR-605-3p which targeted VANGL1 in BC cells. Through repressing miR-605-3p availability, circ-VANGL1 contributes to VANGL1 expression, consequently leading to BC cell proliferation, migration, and invasion. Taken together, our study demonstrated circ-VANGL1/miR-605-3p/VANGL1 as a novel essential signaling pathway involved in BC progression.