BackgroundStudents in secondary vocational health school are at the age of puberty and prone to depressive symptoms. Peer victimization and social media addiction are found to be crucial in influencing the development of depression， and positive mental health has been proven to alleviate depressive symptoms， whereas there remains a striking lack of research on the mediating role of positive mental health and social media addiction in the relationship between peer victimization and depressive symptoms among secondary vocational health school students. ObjectiveTo explore the relationship between peer victimization and depressive symptoms and investigate the mediating role of positive mental health and social media addiction， so as to provide references for the prevention of depression among secondary vocational health school students. MethodsFrom October to December 2020， a cluster sampling framework was utilized to recruit 7 307 students from a secondary vocational health school in Luzhou City， Sichuan Province. Assessments were performed using Multidimensional Peer Victimization Scale （MPVS）， Warwick-Edinburgh Mental Well-being Scale （WEMWBS）， Bergen Social Media Addiction Scale （BSMAS） and Patient Health Questionnaire Depression Scale-9 item （PHQ-9）. Spearman correlation analysis was calculated to determine correlations between scores of scales， Process 4.0 was employed to test the mediation effect， and the bias-corrected Bootstrap procedure was used to test the significance of the mediation effect. ResultsA total of 7 044 （96.40%） valid questionnaires were collected. And 4 391（62.34%）students were found to have depressive symptoms. Correlation analysis revealed that PHQ-9 score was positively correlated with BSMAS score and MPVS score （r=0.404， 0.506， P<0.01）. WEMWBS score was negatively correlated with PHQ-9 score， BSMAS score and MPVS score （r=-0.587， -0.259， -0.358， P<0.01）. BSMAS score was positively correlated with MPVS score （r=0.328， P<0.01）. Positive mental health played a mediating role in the relationship between peer victimization and depressive symptoms， with an indirect effect value of 0.130 （95% CI： 0.119~0.141）， accounting for 30.81% of the total effect. Social media addiction also mediated the relationship between peer victimization and depressive symptoms， with an indirect effect value of 0.052 （95% CI： 0.045~0.059）， accounting for 12.34% of the total effect. Positive mental health and social media addiction exhibited a chained mediation effect on the relationship between peer victimization and depressive symptoms， with an indirect effect value of 0.012 （95% CI： 0.010~0.014） and accounting for 2.84% of the total effect. ConclusionPeer victimization can affect the presence of depressive symptoms among secondary vocational health school students both directly and indirectly through either separate or chained mediation of positive mental health and social media addiction.

Sensorineural hearing loss (SNHL), the most commonly-occurring form of hearing loss, is caused mainly by injury to or the loss of hair cells and spiral ganglion neurons in the cochlea. Numerous environmental and physiological factors have been shown to cause acquired SNHL, such as ototoxic drugs, noise exposure, aging, infections, and diseases. Several programmed cell death (PCD) pathways have been reported to be involved in SNHL, especially some novel PCD pathways that have only recently been reported, such as ferroptosis, necroptosis, and pyroptosis. Here we summarize these PCD pathways and their roles and mechanisms in SNHL, aiming to provide new insights and potential therapeutic strategies for SNHL by targeting these PCD pathways.
Humans ; Hearing Loss, Sensorineural/metabolism* ; Necroptosis/drug effects* ; Pyroptosis/drug effects* ; Ferroptosis/drug effects* ; Animals

Tumor cells adapt their metabolism to meet the demands for energy and biosynthesis.Mitochondria,pivotal organelles in the metabolic reprogramming of tumor cells,contribute to tumorigenesis and cancer progression significantly through various dysfunctions in both tumor and immune cells.Alterations in mitochondrial dynamics and metabolic signaling pathways exert crucial regulatory influence on the activation,proliferation,and differentiation of immune cells.The tumor microenvironment orchestrates the activation and functionality of tumor-infiltrating immune cells by reprogramming mitochondrial metabolism and inducing shifts in mitochondrial dynamics,thereby facilitating the establishment of a tumor immunosuppressive microenvironment.Stress-induced leakage of mitochondrial DNA contributes multifaceted regulatory effects on anti-tumor immune responses and the immunosuppressive microenvironment by activating multiple natural immune signals,including cGAS-STING,TLR9,and NLRP3.Moreover,mitochondrial DNA-mediated immunogenic cell death emerges as a promising avenue for anti-tumor immunotherapy.Additionally,mitochondrial reactive oxygen species,a crucial factor in tumorigenesis,drives the formation of tumor immunosuppressive microenvironment by changing the composition of immune cells within the tumor microenvironment.This review focuses on the intrinsic relationship between mitochondrial biology and anti-tumor immune responses from multiple angles.We explore the core role of mitochondria in the dynamic interplay between the tumor and the host to facilitate the development of targeted mitochondrial strategies for anti-tumor immunotherapy.

Tumor cells adapt their metabolism to meet the demands for energy and biosynthesis.Mitochondria,pivotal organelles in the metabolic reprogramming of tumor cells,contribute to tumorigenesis and cancer progression significantly through various dysfunctions in both tumor and immune cells.Alterations in mitochondrial dynamics and metabolic signaling pathways exert crucial regulatory influence on the activation,proliferation,and differentiation of immune cells.The tumor microenvironment orchestrates the activation and functionality of tumor-infiltrating immune cells by reprogramming mitochondrial metabolism and inducing shifts in mitochondrial dynamics,thereby facilitating the establishment of a tumor immunosuppressive microenvironment.Stress-induced leakage of mitochondrial DNA contributes multifaceted regulatory effects on anti-tumor immune responses and the immunosuppressive microenvironment by activating multiple natural immune signals,including cGAS-STING,TLR9,and NLRP3.Moreover,mitochondrial DNA-mediated immunogenic cell death emerges as a promising avenue for anti-tumor immunotherapy.Additionally,mitochondrial reactive oxygen species,a crucial factor in tumorigenesis,drives the formation of tumor immunosuppressive microenvironment by changing the composition of immune cells within the tumor microenvironment.This review focuses on the intrinsic relationship between mitochondrial biology and anti-tumor immune responses from multiple angles.We explore the core role of mitochondria in the dynamic interplay between the tumor and the host to facilitate the development of targeted mitochondrial strategies for anti-tumor immunotherapy.

Tumor cells adapt their metabolism to meet the demands for energy and biosynthesis.Mitochondria,pivotal organelles in the metabolic reprogramming of tumor cells,contribute to tumorigenesis and cancer progression significantly through various dysfunctions in both tumor and immune cells.Alterations in mitochondrial dynamics and metabolic signaling pathways exert crucial regulatory influence on the activation,proliferation,and differentiation of immune cells.The tumor microenvironment orchestrates the activation and functionality of tumor-infiltrating immune cells by reprogramming mitochondrial metabolism and inducing shifts in mitochondrial dynamics,thereby facilitating the establishment of a tumor immunosuppressive microenvironment.Stress-induced leakage of mitochondrial DNA contributes multifaceted regulatory effects on anti-tumor immune responses and the immunosuppressive microenvironment by activating multiple natural immune signals,including cGAS-STING,TLR9,and NLRP3.Moreover,mitochondrial DNA-mediated immunogenic cell death emerges as a promising avenue for anti-tumor immunotherapy.Additionally,mitochondrial reactive oxygen species,a crucial factor in tumorigenesis,drives the formation of tumor immunosuppressive microenvironment by changing the composition of immune cells within the tumor microenvironment.This review focuses on the intrinsic relationship between mitochondrial biology and anti-tumor immune responses from multiple angles.We explore the core role of mitochondria in the dynamic interplay between the tumor and the host to facilitate the development of targeted mitochondrial strategies for anti-tumor immunotherapy.

Tumor cells adapt their metabolism to meet the demands for energy and biosynthesis.Mitochondria,pivotal organelles in the metabolic reprogramming of tumor cells,contribute to tumorigenesis and cancer progression significantly through various dysfunctions in both tumor and immune cells.Alterations in mitochondrial dynamics and metabolic signaling pathways exert crucial regulatory influence on the activation,proliferation,and differentiation of immune cells.The tumor microenvironment orchestrates the activation and functionality of tumor-infiltrating immune cells by reprogramming mitochondrial metabolism and inducing shifts in mitochondrial dynamics,thereby facilitating the establishment of a tumor immunosuppressive microenvironment.Stress-induced leakage of mitochondrial DNA contributes multifaceted regulatory effects on anti-tumor immune responses and the immunosuppressive microenvironment by activating multiple natural immune signals,including cGAS-STING,TLR9,and NLRP3.Moreover,mitochondrial DNA-mediated immunogenic cell death emerges as a promising avenue for anti-tumor immunotherapy.Additionally,mitochondrial reactive oxygen species,a crucial factor in tumorigenesis,drives the formation of tumor immunosuppressive microenvironment by changing the composition of immune cells within the tumor microenvironment.This review focuses on the intrinsic relationship between mitochondrial biology and anti-tumor immune responses from multiple angles.We explore the core role of mitochondria in the dynamic interplay between the tumor and the host to facilitate the development of targeted mitochondrial strategies for anti-tumor immunotherapy.

Tumor cells adapt their metabolism to meet the demands for energy and biosynthesis.Mitochondria,pivotal organelles in the metabolic reprogramming of tumor cells,contribute to tumorigenesis and cancer progression significantly through various dysfunctions in both tumor and immune cells.Alterations in mitochondrial dynamics and metabolic signaling pathways exert crucial regulatory influence on the activation,proliferation,and differentiation of immune cells.The tumor microenvironment orchestrates the activation and functionality of tumor-infiltrating immune cells by reprogramming mitochondrial metabolism and inducing shifts in mitochondrial dynamics,thereby facilitating the establishment of a tumor immunosuppressive microenvironment.Stress-induced leakage of mitochondrial DNA contributes multifaceted regulatory effects on anti-tumor immune responses and the immunosuppressive microenvironment by activating multiple natural immune signals,including cGAS-STING,TLR9,and NLRP3.Moreover,mitochondrial DNA-mediated immunogenic cell death emerges as a promising avenue for anti-tumor immunotherapy.Additionally,mitochondrial reactive oxygen species,a crucial factor in tumorigenesis,drives the formation of tumor immunosuppressive microenvironment by changing the composition of immune cells within the tumor microenvironment.This review focuses on the intrinsic relationship between mitochondrial biology and anti-tumor immune responses from multiple angles.We explore the core role of mitochondria in the dynamic interplay between the tumor and the host to facilitate the development of targeted mitochondrial strategies for anti-tumor immunotherapy.

Tumor cells adapt their metabolism to meet the demands for energy and biosynthesis.Mitochondria,pivotal organelles in the metabolic reprogramming of tumor cells,contribute to tumorigenesis and cancer progression significantly through various dysfunctions in both tumor and immune cells.Alterations in mitochondrial dynamics and metabolic signaling pathways exert crucial regulatory influence on the activation,proliferation,and differentiation of immune cells.The tumor microenvironment orchestrates the activation and functionality of tumor-infiltrating immune cells by reprogramming mitochondrial metabolism and inducing shifts in mitochondrial dynamics,thereby facilitating the establishment of a tumor immunosuppressive microenvironment.Stress-induced leakage of mitochondrial DNA contributes multifaceted regulatory effects on anti-tumor immune responses and the immunosuppressive microenvironment by activating multiple natural immune signals,including cGAS-STING,TLR9,and NLRP3.Moreover,mitochondrial DNA-mediated immunogenic cell death emerges as a promising avenue for anti-tumor immunotherapy.Additionally,mitochondrial reactive oxygen species,a crucial factor in tumorigenesis,drives the formation of tumor immunosuppressive microenvironment by changing the composition of immune cells within the tumor microenvironment.This review focuses on the intrinsic relationship between mitochondrial biology and anti-tumor immune responses from multiple angles.We explore the core role of mitochondria in the dynamic interplay between the tumor and the host to facilitate the development of targeted mitochondrial strategies for anti-tumor immunotherapy.

Tumor cells adapt their metabolism to meet the demands for energy and biosynthesis.Mitochondria,pivotal organelles in the metabolic reprogramming of tumor cells,contribute to tumorigenesis and cancer progression significantly through various dysfunctions in both tumor and immune cells.Alterations in mitochondrial dynamics and metabolic signaling pathways exert crucial regulatory influence on the activation,proliferation,and differentiation of immune cells.The tumor microenvironment orchestrates the activation and functionality of tumor-infiltrating immune cells by reprogramming mitochondrial metabolism and inducing shifts in mitochondrial dynamics,thereby facilitating the establishment of a tumor immunosuppressive microenvironment.Stress-induced leakage of mitochondrial DNA contributes multifaceted regulatory effects on anti-tumor immune responses and the immunosuppressive microenvironment by activating multiple natural immune signals,including cGAS-STING,TLR9,and NLRP3.Moreover,mitochondrial DNA-mediated immunogenic cell death emerges as a promising avenue for anti-tumor immunotherapy.Additionally,mitochondrial reactive oxygen species,a crucial factor in tumorigenesis,drives the formation of tumor immunosuppressive microenvironment by changing the composition of immune cells within the tumor microenvironment.This review focuses on the intrinsic relationship between mitochondrial biology and anti-tumor immune responses from multiple angles.We explore the core role of mitochondria in the dynamic interplay between the tumor and the host to facilitate the development of targeted mitochondrial strategies for anti-tumor immunotherapy.