Testicular aging manifests as impaired spermatogenesis and morphological alterations in Drosophila. Nonetheless, the comprehensive molecular regulatory framework remains largely undisclosed. This investigation illustrates the impact of copper overload on testicular aging and underscores the interplay between copper overload and lncRNA. Copper overload triggers Cuproptosis through the mitochondrial TCA cycle, facilitating intracellular interactions with Ferroptosis, thereby governing testicular aging. Dysfunction of lncRNA:CR43306 also contributes to testicular aging in Drosophila, emphasizing the significance of lncRNA:CR43306 as a novel aging-associated lncRNA. Moreover, copper overload exacerbates spermatid differentiation defects mediated by lncRNA:CR43306 deficiency through oxidative stress, copper, and iron transport. Therapeutically, Ferrostatin-1 and Resveratrol emerge as potential remedies for addressing testicular aging. This study offers perspectives on the regulatory mechanisms involving copper overload and lncRNA:CR43306 deficiency in the context of testicular aging.

中文翻译：

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果蝇中铜超载通过 lncRNA:CR43306 缺乏通过铁死亡介导睾丸衰老


睾丸衰老表现为果蝇精子发生受损和形态改变。尽管如此，全面的分子调控框架在很大程度上仍未公开。这项研究说明了铜超载对睾丸衰老的影响，并强调了铜超载与 lncRNA 之间的相互作用。铜超载通过线粒体 TCA 循环触发 Cuprotosis，促进细胞内与 Ferroptosis 的相互作用，从而控制睾丸衰老。 lncRNA:CR43306的功能障碍也导致果蝇睾丸衰老，这强调了lncRNA:CR43306作为一种新型的衰老相关lncRNA的重要性。此外，铜超载会通过氧化应激、铜和铁转运加剧 lncRNA:CR43306 缺乏介导的精子细胞分化缺陷。在治疗上，Ferrostatin-1 和白藜芦醇成为解决睾丸衰老问题的潜在疗法。这项研究为睾丸衰老背景下铜超载和 lncRNA:CR43306 缺乏的调节机制提供了视角。