Peptide Angio-3 Attenuates Pulmonary Fibrosis Via Modulation of the Coagulation Factor Xa-Protease-Activated Receptor-1 Signaling Axis.
A new study published in FASEB Journal highlights the potential of the peptide Angio-3 in combating pulmonary fibrosis (PF). This chronic lung disease is notorious for its severe impact on respiratory function and has limited therapeutic options. Researchers led by Wang et al. from North Sichuan Medical College and other institutions have identified Angio-3 as a promising antifibrotic agent.
FASEB J
by Wang D, Li F, Chen H et al.
“Peptide Angio-3 Attenuates Pulmonary Fibrosis Via Modulation of the Coagulation Factor Xa-Protease-Activated Receptor-1 Signaling Axis. Wang D(1), Li F(1), Chen H(2), Deng B(3), Cheng L(4), Ma J(2), Li R(2), Qu L(5), Xie J(3), Zhao Y(2). Author information: (1)Institute of Basic Medicine, North Sichuan Medical College, Nanchong, Sichuan, China. (2)Medical School of Ophthalmology and Optometry, North Sichuan Medical College, Nanchong, Sichuan, China. (3)Key Laboratory of Preclinical Study for New Drugs of Gansu Province, School of Basic Medical Sciences & Research Unit of Peptide Science, Chinese Academy of Medical Sciences, 2019RU066, Lanzhou University, Lanzhou, China. (4)School of Biomedical Engineering, Shenzhen University Health Science Center, Shenzhen University, Shenzhen, China. (5)School of Pharmacy, North Sichuan Medical College, Nanchong, Sichuan, China. Pulmonary fibrosis (PF) is a chronic, progressive, and often fatal interstitial lung disease characterized by interstitial remodeling, fibroblastic foci formation, and excessive extracellular matrix (ECM) deposition. Current therapeutic options remain limited and are associated with unfavorable prognoses. Growing evidence indicates that dysregulated coagulation and fibrinolytic pathways are intimately involved in its pathology, suggesting that modulating this axis may offer novel therapeutic opportunities. In this study, we characterize Angio-3, a plasminogen kringle 3-derived decapeptide, as a potential antifibrotic agent targeting the coagulation cascade. We aimed to investigate the therapeutic efficacy of Angio-3 and elucidate its underlying mechanism. Our results show that Angio-3 significantly alleviates PF by inhibiting fibroblast invasion and migration and functions as a protease-activated receptor-1 (PAR-1) antagonist that disrupts the coagulation factor Xa (FXa)-PAR-1 signaling axis. Toxicological evaluations revealed a favorable safety profile, with no adverse effects observed at 0.5 mg/kg/day and only mild hepatomegaly at a supratherapeutic dose. These findings identify Angio-3 as a promising therapeutic candidate with dual advantages-combining antifibrotic efficacy with low toxicity-and offer a novel strategy for treating PF through targeting coagulation-mediated fibrotic signaling. © 2026 The Author(s). The FASEB Journal published by Wiley Periodicals LLC on behalf of Federation of American Societies for Experimental Biology.”
Angio-3, derived from plasminogen kringle 3, works by modulating the coagulation factor Xa and protease-activated receptor-1 (PAR-1) signaling axis. The study demonstrates that Angio-3 significantly reduces fibroblast invasion and migration, key processes in the development of PF. By acting as a PAR-1 antagonist, it disrupts pathways that contribute to the disease's progression.
Key findings from the research include:
Angio-3 effectively alleviates pulmonary fibrosis symptoms.
It targets the coagulation cascade, offering a novel therapeutic avenue.
The peptide displayed a favorable safety profile, with no major adverse effects at a dose of 0.5 mg/kg/day.
Only mild hepatomegaly was observed at higher doses, indicating low toxicity.
The results are promising for patients suffering from PF, suggesting that Angio-3 could offer both antifibrotic benefits and a safer profile compared to existing treatments. This research not only advances our understanding of PF but also opens new doors for peptide-based therapies in managing this challenging condition.
Overall, Angio-3 marks a significant step forward in peptide research, providing hope for better treatment strategies in pulmonary fibrosis.
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