PulseExploreJournal ClubDebatesTrendingResearchersJournals
Instagram
HomeExploreJournal ClubTrending
Synapse
⌘+K
Synapse
April 11, 2026ACS Nano1 citations

A Lung-Targeted Carrier of Carbon Monoxide for Idiopathic Pulmonary Fibrosis Therapy

View Full Paper
WGWenyu GuoArtificial Intelligence in Medicine (Canada)SHShuo HuangJZJiabin ZhangPeking University

Key Points

  • The aim is to develop a lung-targeted carrier for carbon monoxide to improve therapy for idiopathic pulmonary fibrosis (IPF).
  • Developed a lung-targeted carbon monoxide carrier (LTCoCO) using phospholipid microspheres.
  • Utilized selective organ targeting principles for efficient delivery.
  • Evaluated in vivo effects on bleomycin-induced pulmonary fibrosis.
  • Conducted mechanistic in vitro studies on signaling pathways involved.
  • LTCoCO demonstrated significant inhibition of IPF in vivo.
  • Resulted in recovery from bleomycin-induced pulmonary fibrosis.
  • In vitro studies showed inhibition of epithelial-mesenchymal transition and fibroblast activation through TGF-β1 pathways.

Abstract

Idiopathic Pulmonary Fibrosis (IPF) is a severely irreversible chronic disease affecting approximately 3 million individuals worldwide, with its pathogenic mechanisms remaining incompletely elucidated. Currently, treatment options of IPF are very limited, with only two FDA-approved drugs. The development of innovative therapeutics and advanced delivery technologies represents a pivotal step to overcoming the current clinical challenges of IPF. CO-based gas therapy is recognized as a potential IPF therapeutic strategy. However, a safe and efficient delivery of CO to pulmonary fibrosis tissue remains a challenge, constraining advancements in this field. To address the above issues, a lung-targeted carrier of CO (LTCoCO) was developed in this study by directly encapsulating CO within phospholipid microspheres, leveraging size-dependent pulmonary retention and selective organ targeting (SORT) principles. By regulating the TGF-β1/Smad signaling pathway and exerting anti-inflammatory, antioxidant, and antifibrotic activities, LTCoCOs have demonstrated in vivo inhibition of IPF, resulting in significant recovery from bleomycin-induced pulmonary fibrosis. Mechanistic in vitro studies identified LTCoCOs as potent inhibitors of epithelial-mesenchymal transition (EMT), endothelial-to-mesenchymal transition (E(nd)MT), and fibroblast activation (FA), acting through both canonical and noncanonical TGF-β1 pathways to achieve robust antifibrotic effects. In summary, an LTCoCO-based strategy for IPF inhibition has been established. These findings expand treatment options and provide a theoretical framework for the IPF clinical application of gas therapy.

Ask AI
Helpful
Bookmark
Share
View Full Paper

Cite This Study

Guo et al. (2026) studied this question.

synapsesocial.com/papers/69d9e58f78050d08c1b75bc0https://doi.org/10.1021/acsnano.6c01762
Ask AI
Helpful
Bookmark
Share
View Full Paper

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Time‐ and compartment‐resolved proteome profiling of the extracellular niche in lung injury and repair2015 · 271 citations
  2. 2Ultrasound contrast agents: microbubbles made simple for the pediatric radiologist2021 · 54 citations
  3. 3Selective organ targeting (SORT) nanoparticles for tissue-specific mRNA delivery and CRISPR–Cas gene editing2020 · 2,325 citations
  4. 4Idiopathic pulmonary fibrosis2017 · 2,059 citations
  5. 5Complex networks orchestrate epithelial–mesenchymal transitions2006 · 3,950 citations