ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024
Supramolecular Nanofibers Ameliorate Bleomycin-Induced Pulmonary Fibrosis by Restoring Autophagy.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- TRPML1 agonist ML-SA5 attenuates pulmonary fibroblast activation by suppressing mTOR and restoring autophagic flux.FEBS open bio · 2026Article
- Synergistic regulation of TGF-β1/Smad2/3 signaling and inflammatory pathways via SA/NAC-based nanoplatforms: a novel strategy to enhance anti-fibrotic therapeutic outcomes in idiopathic pulmonary fibrosis.Journal of nanobiotechnology · 2026Article
- Self-assembling peptide inspired by insulin and type 1 insulin-like growth factor for the treatment of androgenetic alopecia.Bioactive materials · 2025Article
- Chiral gold nanoparticles manipulate osteoimmune microenvironment via macrophage autophagy for bone regeneration.Materials today. Bio · 2025Article
- Autophagy and exosome dynamics in Radiation-Induced pulmonary fibrosis: the critical role of TRIB3.Respiratory research · 2025Article
- MDA5 protein mediating persistent ER stress/unfolded protein response contributes to endothelial-mesenchymal-transition of lung microvascular endothelial cell in dermatomyositis.Cell communication and signaling : CCS · 2025Article
- Mechanisms and Therapeutic Potential of Myofibroblast Transformation in Pulmonary Fibrosis.Journal of respiratory biology and translational medicine · 2025Article
- Review
- The histone demethylase KDM6B links obstructive sleep apnea to idiopathic pulmonary fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Supramolecular Nanofibers Ameliorate Bleomycin-Induced Pulmonary Fibrosis by Restoring Autophagy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Understanding the molecular regulatory mechanisms of autophagy in lung disease pathogenesis.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive and ultimately fatal interstitial lung disease, with limited therapeutic options available. Impaired autophagy resulting from aberrant TRB3/p62 protein-protein interactions (PPIs) contributes to the progression of IPF. Restoration of autophagy by modulating the TRB3/p62 PPIs has rarely been reported for the treatment of IPF. Herein, peptide nanofibers are developed that specifically bind to TRB3 protein and explored their potential as a therapeutic approach for IPF. By conjugating with the self-assembling fragment (Ac-GFFY), a TRB3-binding peptide motif A2 allows for the formation of nanofibers with a stable α-helix secondary structure. The resulting peptide (Ac-GFFY-A2) nanofibers exhibit specific high-affinity binding to TRB3 protein in saline buffer and better capacity of cellular uptake to A2 peptide. Furthermore, the TRB3-targeting peptide nanofibers efficiently interfere with the aberrant TRB3/p62 PPIs in activated fibroblasts and fibrotic lung tissue of mice, thereby restoring autophagy dysfunction. The TRB3-targeting peptide nanofibers inhibit myofibroblast differentiation, collagen production, and fibroblast migration in vitro is demonstrated, as well as bleomycin-induced pulmonary fibrosis in vivo. This study provides a supramolecular method to modulate PPIs and highlights a promising strategy for treating IPF diseases by restoring autophagy.
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