Prasugrel inhibits TLR7-driven autoimmunity in systemic lupus erythematosus by acetylating cGAS

Z Zeng-Lin Guo L Li-Ming Sun S Shuai Jiang (State Key Laboratory of Chemical Reaction Dynamics and Dalian Coherent Light Source, Dalian Institute of Chemical Physics) M Ming Zhao Y Yuhui Li (Department of Rheumatology and Immunology, Peking University People’s Hospital) J Jinjing Qian Y Yakai Fu C Chunmei Wu Y Ying Yuan W Wen Xue S Shao-Zhen Jiang S Sen-Chao Yuan X Xucheng Lv X Xingxing Yang (Key Laboratory of Biomass Chemical Engineering of Ministry of Education, College of Chemical and Biological Engineering) L Lehua Yin P Peng-Peng Zhu Y Yu Yu X Xin Xu K Kai Wang Q Qiu-Ying Han Z Zhuoxin Li Z Zhi-Hui Su X Xi-Ping Yu J Jiaqi Wu H Hong Cai T Tian Xia Y Yuan Chen (School of Chemical and Biomolecular Engineering) X Xue-Min Zhang W Wei-Hua Li A Ai-Ling Li T Tao Zhou (College of Life Sciences, University of Chinese Academy of Sciences, Beijing, China.) Z Zhanguo Li Q Qiong Fu X Xinhua He (Institute of Eco-environment and Industrial Technology, Shanxi Agricultural University) T Tao Li

Abstract

Abstract Systemic lupus erythematosus (SLE) has a complex, multifactorial etiology, which contributes to a lack of definitive cure and limited treatment efficacy. Here, we report that cyclic GMP-AMP synthase (cGAS) is significantly activated in SLE patients. We further demonstrate that cGAS deletion protects mice from lupus-like symptoms induced by the TLR7 agonist imiquimod (IMQ). In a screen of 3,159 FDA-approved drugs, we identify the antiplatelet agent prasugrel as a potent cGAS inhibitor. Mechanistically, prasugrel disrupts the DNA-triggered liquid phase condensation and activation of cGAS via direct acetylation. Strikingly, we find that prasugrel exhibits remarkable efficacy in treating SLE in both mouse models and patient cells. Importantly, we report elevated plasma cyclic GMP-AMP (cGAMP) in SLE patients and identify it as a potential biomarker for predicting prasugrel response. Thus, our work elucidates the essential role of cGAS in SLE pathogenesis and presents prasugrel as a promising therapeutic option with immediate translational potential.

Article Details

Volume / Issue Vol. 17, Issue 1
Published March 18, 2026
ISSN 2041-1723
Publisher Nature Portfolio

Journal Info

Nature Communications

Nature Portfolio

ISSN: 2041-1723 Open Access Life Sciences

Authors (35)

Z

Zeng-Lin Guo

L

Li-Ming Sun

S

Shuai Jiang

State Key Laboratory of Chemical Reaction Dynamics and Dalian Coherent Light Source, Dalian Institute of Chemical Physics

M

Ming Zhao

Y

Yuhui Li

Department of Rheumatology and Immunology, Peking University People’s Hospital

J

Jinjing Qian

Y

Yakai Fu

C

Chunmei Wu

Y

Ying Yuan

W

Wen Xue

S

Shao-Zhen Jiang

S

Sen-Chao Yuan

X

Xucheng Lv

X

Xingxing Yang

Key Laboratory of Biomass Chemical Engineering of Ministry of Education, College of Chemical and Biological Engineering

L

Lehua Yin

P

Peng-Peng Zhu

Y

Yu Yu

X

Xin Xu

K

Kai Wang

Q

Qiu-Ying Han

Z

Zhuoxin Li

Z

Zhi-Hui Su

X

Xi-Ping Yu

J

Jiaqi Wu

H

Hong Cai

T

Tian Xia

Y

Yuan Chen

School of Chemical and Biomolecular Engineering

X

Xue-Min Zhang

W

Wei-Hua Li

A

Ai-Ling Li

T

Tao Zhou

College of Life Sciences, University of Chinese Academy of Sciences, Beijing, China.

Z

Zhanguo Li

Q

Qiong Fu

X

Xinhua He

Institute of Eco-environment and Industrial Technology, Shanxi Agricultural University

T

Tao Li