ArticleMolecular and cellular biochemistry2026
USP35-mediated NRF2 deubiquitination attenuates experimental cryptorchidism-induced testicular damage and H
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Cryptorchidism, characterized by the failure of one or both testes to descend into the scrotum, is the most prevalent urogenital malformation in male infants and an important risk element of male infertility and testicular cancer. The purpose of this study was to investigate the molecular mechanisms underlying cryptorchidism-induced testicular damage, with a focus on the role of USP35. Here we established a unilateral experimental cryptorchidism model of Sprague-Dawley rats by resetting the left testis to the abdominal cavity and suturing the inguinal canal, thus preventing its natural descent. The findings indicated that apoptosis and oxidative stress (OS) levels were increased in the undescended testis (UDT) compared to the descended testis (DT) group. Subsequent mRNA sequencing of DT and UDT tissues revealed that ubiquitin specific peptidase 35 (USP35) expression was downregulated in the UDT, implying that USP35 may be an important factor in the pathogenesis of cryptorchidism. To further investigate, an oxidative damage model was constructed using H
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