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ABSTRACTBackground: Music therapy is increasingly examined in randomized controlled trials (RCTs) and shows potential in treating post-traumatic stress disorder (PTSD).Objective: This systematic review and meta-analysis critically evaluates the current clinical evidence supporting the efficacy and acceptability of music therapy for PTSD.Method: RCTs comparing music therapy in addition to care as usual (CAU) versus either CAU alone or CAU combined with standard psychotherapy/pharmacotherapy for PTSD were retrieved from major English – and Chinese-language databases. Standardized mean differences (SMDs) for post-treatment PTSD symptom scores and risk differences (RDs) for retention rates upon treatment completion were calculated to assess the efficacy and acceptability of music therapy, respectively. The Cochrane risk of bias (RoB) tool 2.0 and the Grading of Recommendations, Assessment, Development, and Evaluations (GRADE) were used to assess the RoB of included studies and certainty of the evidence, respectively.Results: Nine studies, incorporating 527 PTSD patients, were included, all with high RoB. The post-treatment PTSD symptom scores were significantly lower in the music therapy group than the inactive control group (SMD = −1.64, P

ABSTRACTRenal proximal tubular cells are highly vulnerable to different types of assaults during filtration and reabsorption, leading to acute renal dysfunction and eventual chronic kidney diseases (CKD). The chemotherapeutic drug cisplatin elicits cytotoxicity causing renal tubular cell death, but its executing mechanisms of action are versatile and elusive. Here, we show that cisplatin induces renal tubular cell apoptosis and ferroptosis by disrupting glutathione (GSH) metabolism. Upon cisplatin treatment, GSH metabolism is impaired leading to GSH depletion as well as the execution of mitochondria-mediated apoptosis and lipid oxidation-related ferroptosis through activating IL6/JAK/STAT3 signaling. Inhibition of JAK/STAT3 signaling reversed cell apoptosis and ferroptosis in response to cisplatin induction. Using a cisplatin-induced acute kidney injury (CAKI) mouse model, we found that inhibition of JAK/STAT3 significantly mitigates cisplatin nephrotoxicity with a reduced level of serum BUN and creatinine as well as proximal tubular distortion. In addition, the GSH booster baicalein also reclaims cisplatin-induced renal tubular cell apoptosis and ferroptosis as well as the in vivo nephrotoxicity. In conclusion, cisplatin disrupts glutathione metabolism, leading to renal tubular cell apoptosis and ferroptosis. Rewiring glutathione metabolism represents a promising strategy for combating cisplatin nephrotoxicity.