Histidine triad nucleotide-binding protein 2 attenuates doxorubicin-induced cardiotoxicity through restoring lysosomal function and promoting autophagy in mice.

• Tác giả: Suling Ding, Zhen Dong, Jinfeng Gao, Junbo Ge, Luna He, Kai Hu, Daile Jia, Hao Jiang, Liwei Liu, Tiantong Ou, Yiqin Shi, Aijun Sun, Xiaolei Sun, Wenlong Yang, Beijian Zhang, Jinyan Zhang
• Ngôn ngữ: eng
• Ký hiệu phân loại: 305.568 +Alienated and excluded classes
• Thông tin xuất bản: China : MedComm , 2025
• Bộ sưu tập: NCBI
• ID: 213553

Tóm tắt

Doxorubicin (DOX) is an effective chemotherapy drug widely used against various cancers but is limited by severe cardiotoxicity. Mitochondria-lysosome interactions are crucial for cellular homeostasis. This study investigates the role of histidine triad nucleotide-binding protein 2 (HINT2) in DOX-induced cardiotoxicity (DIC). We found that HINT2 expression was significantly upregulated in the hearts of DOX-treated mice. Cardiac-specific