文献类型：期刊文献

英文题名：Integrated Multiomic Analysis Reveals the Therapeutic Potential of Danhong Injection in Mitigating Radiation-Induced Heart Disease by Modulating Ferroptosis

作者：Wang, Bo-wen[1,2];Wang, Gang[3];Zhang, Zhan[2];Lu, Wei-jie[1];Li, Yan-ling[1,2];Shu, Yan-biao[4];Xie, Ping[1,2,3,4]

第一作者：Wang, Bo-wen

通信作者：Xie, P[1];Xie, P[2];Xie, P[3];Xie, P[4]

机构：[1]Gansu Univ Chinese Med, Sch Tradit Chinese & Western Med, Lanzhou, Peoples R China;[2]Gansu Prov Hosp, Dept Cardiovasc Med, Lanzhou, Peoples R China;[3]Lanzhou Univ, Sch Clin Med 1, Lanzhou, Peoples R China;[4]Gansu Univ Chinese Med, Clin Med Coll 1, Lanzhou, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Sch Tradit Chinese & Western Med, Lanzhou, Peoples R China;[2]corresponding author), Gansu Prov Hosp, Dept Cardiovasc Med, Lanzhou, Peoples R China;[3]corresponding author), Lanzhou Univ, Sch Clin Med 1, Lanzhou, Peoples R China;[4]corresponding author), Gansu Univ Chinese Med, Clin Med Coll 1, Lanzhou, Peoples R China.|[10735]甘肃中医药大学;

年份：2025

卷号：39

期号：19

外文期刊名：FASEB JOURNAL

收录：;Scopus(收录号：2-s2.0-105018288028);WOS:【SCI-EXPANDED(收录号:WOS:001591087800001)】；

基金：This work was supported by grants from the National Natural Science Foundation of China (No. 82460051), the Major Project of Gansu Province Joint Research Fund (No. 24JRRA886), the Natural Science Foundation of Gansu Province (No. 23JRRA1287), and the Gansu Provincial Hospital Internal Fund Project (22GSSYD-14).

语种：英文

摘要：Radiation-induced heart disease (RIHD) has garnered increasing clinical attention. While oxidative stress plays a pivotal role in RIHD pathogenesis and progression, the involvement of ferroptosis-a regulated cell death pathway closely linked to oxidative stress-remains poorly characterized. Danhong injection (DHI), a clinically approved traditional Chinese medicine, is widely used for treating cardiovascular disorders because of its anti-inflammatory and antioxidant properties. Therefore, we investigated whether DHI exerts therapeutic effects against RIHD by suppressing ferroptosis. We established both in vivo and in vitro RIHD models. Ferrostatin-1 (Fer-1), a selective ferroptosis inhibitor, was used as a positive control. Mice and cardiomyocytes (H9C2 and AC16 cell lines) were treated with DHI postirradiation. Myocardial tissue/cellular/mitochondrial damage was comprehensively assessed through histopathological and functional analyses. Oxidative/antioxidant imbalance was quantified via biochemical assays, and ferroptosis-related protein expression was evaluated using immunohistochemistry and Western blotting. Finally, transcriptomic and metabolomic sequencing, coupled with bioinformatics approaches, was performed using murine myocardial tissues to elucidate molecular alterations. X-irradiation induced structural and functional damage in myocardial tissues and cells, accompanied by oxidative stress and ferroptosis activation. DHI treatment significantly mitigated those effects, restoring myocardial integrity and viability. Differentially expressed genes and metabolites were predominantly enriched in immune response pathways and metabolic reprogramming processes. Promising RNA-metabolite interactions that may serve as therapeutic targets for future investigations were revealed. DHI ameliorates RIHD by inhibiting ferroptosis. Integrated multiomics not only validated the therapeutic potential of DHI but also provided novel insights into the molecular mechanisms underlying radiation-induced cardiac injury.