Peptide Angio-3 Attenuates Pulmonary Fibrosis Via Modulation of Coagulation Factor Xa-PAR-1 Signaling Axis
Wang D, Li F, Chen H, Deng B, Cheng L, Ma J, Li R, Qu L, Xie J, Zhao Y
Summary
Angio-3, a 10-residue peptide derived from human plasminogen kringle 3, demonstrated significant antifibrotic activity in pulmonary fibrosis models by functioning as a PAR-1 antagonist that disrupts the coagulation factor Xa-PAR-1 signaling axis. The peptide inhibited fibroblast invasion and migration with a favorable safety profile—no adverse effects at 0.5 mg/kg/day and only mild hepatomegaly at supratherapeutic doses.
Clinical Significance
Current pulmonary fibrosis treatments (pirfenidone, nintedanib) have limited efficacy and significant side effects. Angio-3's dual mechanism—combining antifibrotic activity with coagulation pathway modulation—represents a novel therapeutic strategy. Its low toxicity profile and targeted action on the FXa-PAR-1 axis position it as a promising candidate for conditions where fibrosis and coagulation dysregulation intersect.
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