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Inhibiting RhoA Activation Via GDP-State Stabilization to Relieve Heart Failure.

通过GDP-状态稳定抑制RhoA激活以缓解心力衰竭。

期刊: Circ Res 日期: 2026-03-20 PMID: 41859798 DOI: 10.1161/CIRCRESAHA.125.327107 浏览: 109
作者: Mengzhu Xue, Yingquan Liang, Zhen Yuan, Xiangning Liu, Longfeng Chang, Yongzhi Wang, Peijia Xu, Tingting Zhang, Hewei Jiang, Zijie Zhao, Jingqiu Liu, Shanshan Ruan, Tianyu Ye, Xuelian Pang, Wenyi Mei, Jiawen Wang, Xiaoqian Sun, Huijuan Wang, Jian Cui, Yao Zu, Xudong Lin, Zhenjiang Zhao, Rui Wang, Hong Huang, Cheng Luo, Shengce Tao, Jing Wang, Yajun Duan, Lili Zhu, Huifang Tang, Jian Zhang, Yong Wang, Chun Li, Honglin Li
Xue, M., Liang, Y., Yuan, Z., Liu, X., Chang, L., Wang, Y., Xu, P., Zhang, T., Jiang, H., Zhao, Z., Liu, J., Ruan, S., Ye, T., Pang, X., Mei, W., Wang, J., Sun, X., Wang, H., Cui, J., . . . Li, H. (2026). Inhibiting RhoA Activation Via GDP-State Stabilization to Relieve Heart Failure.. Circ Res. https://doi.org/10.1161/CIRCRESAHA.125.327107
Xue M, Liang Y, Yuan Z, Liu X, Chang L, Wang Y, et al. Inhibiting RhoA Activation Via GDP-State Stabilization to Relieve Heart Failure.. Circ Res. 2026; doi: 10.1161/CIRCRESAHA.125.327107
Xue M, Liang Y, Yuan Z, et al. Inhibiting RhoA Activation Via GDP-State Stabilization to Relieve Heart Failure.[J]. Circ Res. 2026. DOI: 10.1161/CIRCRESAHA.125.327107.
@article{xue2026,
  author = {Mengzhu Xue and Yingquan Liang and Zhen Yuan and Xiangning Liu and Longfeng Chang and Yongzhi Wang and Peijia Xu and Tingting Zhang and Hewei Jiang and Zijie Zhao and Jingqiu Liu and Shanshan Ruan and Tianyu Ye and Xuelian Pang and Wenyi Mei and Jiawen Wang and Xiaoqian Sun and Huijuan Wang and Jian Cui and Yao Zu and Xudong Lin and Zhenjiang Zhao and Rui Wang and Hong Huang and Cheng Luo and Shengce Tao and Jing Wang and Yajun Duan and Lili Zhu and Huifang Tang and Jian Zhang and Yong Wang and Chun Li and Honglin Li},
  title = {Inhibiting RhoA Activation Via GDP-State Stabilization to Relieve Heart Failure.},
  journal = {Circ Res},
  year = {2026},
  doi = {10.1161/CIRCRESAHA.125.327107},
  note = {PMID: 41859798},
}
TY  - JOUR
AU  - Mengzhu Xue
AU  - Yingquan Liang
AU  - Zhen Yuan
AU  - Xiangning Liu
AU  - Longfeng Chang
AU  - Yongzhi Wang
AU  - Peijia Xu
AU  - Tingting Zhang
AU  - Hewei Jiang
AU  - Zijie Zhao
AU  - Jingqiu Liu
AU  - Shanshan Ruan
AU  - Tianyu Ye
AU  - Xuelian Pang
AU  - Wenyi Mei
AU  - Jiawen Wang
AU  - Xiaoqian Sun
AU  - Huijuan Wang
AU  - Jian Cui
AU  - Yao Zu
AU  - Xudong Lin
AU  - Zhenjiang Zhao
AU  - Rui Wang
AU  - Hong Huang
AU  - Cheng Luo
AU  - Shengce Tao
AU  - Jing Wang
AU  - Yajun Duan
AU  - Lili Zhu
AU  - Huifang Tang
AU  - Jian Zhang
AU  - Yong Wang
AU  - Chun Li
AU  - Honglin Li
TI  - Inhibiting RhoA Activation Via GDP-State Stabilization to Relieve Heart Failure.
T2  - Circ Res
PY  - 2026
DO  - 10.1161/CIRCRESAHA.125.327107
AN  - PMID:41859798
ER  - 

摘要

Given the persistently high morbidity and mortality of heart failure (HF), targeting myocardial remodeling, particularly pathological hypertrophy and fibrosis, has become a major therapeutic priority. RhoA (Ras homolog gene family member A), a small GTPase governing cytoskeletal reorganization and cell migration, plays a pivotal role in this process. However, RhoA has long been considered undruggable because of its high-affinity binding to GDP/GTP and the absence of well-defined druggable pockets. Structural analyses comparing RhoA-GTP and RhoA-GDP conformations, combined with surface plasmon resonance-based screening, were used to identify a RhoA inhibitor. The underlying mechanism was validated in cultured cells and 3-dimensional myocardial tissue models. Therapeutic efficacy was assessed across multiple species of HF models and supported by multiomics analyses linking RhoA activation to human HF. Key findings were further confirmed by multiplex immunohistochemistry and pulldown assays in human heart specimens. We identified an unrecognized cryptic pocket adjacent to GDP in RhoA. A natural product, AH001, selectively occupied this pocket and interacted with GDP, thereby stabilizing the interaction between RhoA and its endogenous inhibitor, RhoGDIα (Rho GDP-dissociation inhibitor 1). AH001 suppressed downstream signaling by reducing MRTFA (myocardin-related transcription factor A) nuclear translocation and downregulating fibrosis- and hypertrophy-related proteins. Moreover, AH001 disrupted pathological crosstalk between These findings establish pharmacological inhibition of RhoA activation as a viable strategy to mitigate myocardial remodeling in HF and provide a conceptual framework for developing reversible inhibitors against previously undruggable small GTPases.

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