Proteomics

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The role HINT2 in DOX-induced cardiac damage

ABSTRACT: This file include 9 sample: heart sample from WT mice (1, 2, 3)+heart sample from WT mice treated with DOX (4,5,6)+heart sample from HINT2 cKO mice treated with DOX (7,8,9))

ORGANISM(S): Mus Musculus

SUBMITTER: Aijun Sun  

PROVIDER: PXD056142 | iProX | Wed Sep 18 00:00:00 BST 2024

REPOSITORIES: iProX

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Publications

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

Jiang Hao H   Zhang Jinyan J   Jia Daile D   Liu Liwei L   Gao Jinfeng J   Zhang Beijian B   Dong Zhen Z   Sun Xiaolei X   Yang Wenlong W   Ou Tiantong T   Ding Suling S   He Luna L   Shi Yiqin Y   Hu Kai K   Sun Aijun A   Ge Junbo J  

MedComm 20250217 3

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 <i>Hint2</i> knockout mice exhibited significantly worse ca  ...[more]

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