Background: This study analyzes and compares the efficacy of using catheter ablation (CA) and traditional drug treatments for atrial fibrillation (AF). Through a systematic review and meta-analysis, it seeks to provide a theoretical basis for using clinical CA for patients with AF.Methods: We searched through articles detailing randomly controlled trials (RCTs) that assessed the surgical effect of CA on the treatment of AF. These articles were published before January 31, 2000 in various English databases, including PubMed, Embase, Medline, Ovid, Springer, and Web of Sciences. The Cochrane Handbook for Systematic Reviews of Intervention 5.0.2 was adopted for the bias risk assessment, and Review Manager 5.3 software was used for the meta-analysis of the articles.Results: A total of 2,098 patients drawn from 13 articles were included in the study. For patients in the experimental group (Exp. group), the meta-analysis showed an increase in the effects of clinical treatment [mean deviation (MD) =3.91; 95% confidence interval (CI), 3.15-4.85; Z=12.36; P<0.00001], an improvement in daily life function (MD =1.45; 95% CI, 1.03-1.87; Z=6.82; P<0.00001), a decrease in body weakness (MD =−2.84; 95% CI, −3.24 to −2.45; Z=14.16; P <0.00001), and an increase in quality of life score (MD =14.15; 95% CI, 7.24-21.05; Z=4.01; P<0.0001). The Exp. group also experienced a reduction
BackgroundOxidative stress and impaired autophagic flux play important roles in the development of peripheral artery disease (PAD). SS31 is considered an important antioxidant peptide and autophagy regulator. We aimed to investigate the role of SS31 in PAD myopathy and its possible mechanism both in vivo and in vitro.MethodsA hind limb ischemia (HLI) model was established with old C57BL/6 (14-month-old) mice. Mice in the SS31 group were intraperitoneally injected with SS31 (3 mg/kg) for 4 weeks. We examined skeletal muscle function and histomorphology, autophagy-related protein levels and reactive oxygen species (ROS) content. For the in vitro experiments, after C2C12 myotubes were treated with CoCl2, SS31, and chloroquine (CQ) or rapamycin (RAPA), we measured ROS content, autophagy-related protein levels and antioxidant enzyme expression.ResultsSS31 treatment effectively enhanced the recovery of skeletal muscle function, alleviated skeletal muscle injury and suppressed mitochondrial ROS production in ischemic limbs. SS31 reduced apoptosis and oxidative stress, and SS31 restored impaired autophagic flux by inhibiting the AKT-mTOR pathway. In vitro studies showed that SS31 restored autophagic flux and improved oxidative stress in C2C12 cells. Moreover, phosphorylated AKT (p-AKT) and phosphorylated mTOR (p-mTOR) levels were reduced.ConclusionThese experiments indicated that SS31 can inhibit oxidative stress by restoring autophagic flux to reverse hypoxia-induced injury in vivo and in vitro.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.