Journal of affective disorders · 2025
Alterations of telomere length and mitochondrial DNA copy number in depressive adolescents with non-suicidal self-injury.
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Wen Dong-Ni, Hu Jia-Hui, Ji Ting, Xiao Xing-Yu, Huang Xin-Chengcheng, Zhang Ji-Fan, Feng Wei-Biao, Zheng Shuo, Xiong Zi-Yi, Hou Cai-Lan
Аннотация
BACKGROUND: NSSI among adolescents is highly prevalent and serves as a significant indicator of subsequent suicidal ideation and behaviors. Recent studies have demonstrated a connection between accelerated cellular aging and a range of psychiatric conditions. The present study explored whether depressive adolescents with NSSI exhibited alterations in telomere length (TL) and mitochondrial DNA copy number (mtDNAcn), both critical markers of cellular aging.
METHODS: The study comprised 70 depressive adolescents with NSSI (84.3 % female) and 34 depressive adolescents without NSSI (61.8 % female). The TL and mtDNAcn were determined by calculating the ratio of telomere repeats to the single-copy gene β-globin, or by measuring the relative quantity of mtDNA compared to β-globin.
RESULTS: In this study, the NSSI group demonstrated significantly shorter TL than the non-NSSI group (P < 0.01). This difference persisted after controlling for age, family history, sex, suicidality, childhood maltreatment, depressive symptoms, and psychotic symptoms (P = 0.005). Furthermore, regression analysis showed that TL was considerably shorter in the female NSSI group than in the non-NSSI group after adjusting for age, family history, suicidality, childhood maltreatment, depressive symptoms, and psychotic symptoms (P < 0.001). After controlling for these variables, mtDNAcn was markedly reduced in the male NSSI group compared to the non-NSSI group (P < 0.001).
CONCLUSIONS: This work is, to our knowledge, the first to demonstrate that NSSI correlates with alterations in TL and mtDNAcn. These findings suggest that molecular pathways associated with aging may play a crucial role in the pathogenesis of NSSI.
METHODS: The study comprised 70 depressive adolescents with NSSI (84.3 % female) and 34 depressive adolescents without NSSI (61.8 % female). The TL and mtDNAcn were determined by calculating the ratio of telomere repeats to the single-copy gene β-globin, or by measuring the relative quantity of mtDNA compared to β-globin.
RESULTS: In this study, the NSSI group demonstrated significantly shorter TL than the non-NSSI group (P < 0.01). This difference persisted after controlling for age, family history, sex, suicidality, childhood maltreatment, depressive symptoms, and psychotic symptoms (P = 0.005). Furthermore, regression analysis showed that TL was considerably shorter in the female NSSI group than in the non-NSSI group after adjusting for age, family history, suicidality, childhood maltreatment, depressive symptoms, and psychotic symptoms (P < 0.001). After controlling for these variables, mtDNAcn was markedly reduced in the male NSSI group compared to the non-NSSI group (P < 0.001).
CONCLUSIONS: This work is, to our knowledge, the first to demonstrate that NSSI correlates with alterations in TL and mtDNAcn. These findings suggest that molecular pathways associated with aging may play a crucial role in the pathogenesis of NSSI.