ArticleScience advances2025
Inhalable myofibroblast targeting nanoparticles for synergistic treatment of pulmonary fibrosis.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed.
- Reconstructing AF-associated atrial fibrosis: Patient-specific iPSC models, fit-for-purpose atrial microphysiological systems, and nanomedicine.Materials today. Bio · 2026Review
- KRAS/ERK2-driven stabilization of AARS1 reprograms tumor metabolism and confers Sorafenib resistance in lung adenocarcinoma.Cell death and differentiation · 2026Article
- Precision nanomedicine for pulmonary diseases: from molecular targeting to clinical translation.Signal transduction and targeted therapy · 2026Review
- Clearing the Pulmonary Traffic Jam With Dual-Enzyme Inhalable Nanoparticles Restore Airflow and Reverse Fibrotic Remodeling.Advanced healthcare materials · 2026Article
- Advances in pharmacotherapy for fibrotic interstitial lung disease.Medical review (2021) · 2026Review
- Liposomal multimodal theranostics for bone disorders: from rational responsive delivery and biomimetic strategies to clinical translation.Journal of nanobiotechnology · 2026Review
- SIRT5-dependent desuccinylation licenses UBR5-mediated degradation of TAMM41 to regulate mitochondrial metabolism in lung adenocarcinoma.Biology direct · 2026Article
- Dual-mechanism inhalable nanocomposite restores the alveolar mucus barrier and enables deep-lesion delivery for synergistic treatment of pulmonary fibrosis.Journal of nanobiotechnology · 2026Article
- Lactylation in tissue fibrosis: epigenetic mechanisms, metabolic crosstalk, and therapeutic opportunities.Journal of translational medicine · 2026Review
- Nanotherapeutic strategies for fibroblast targeted treatment of pulmonary fibrosis.Nanomedicine (London, England) · 2026Article
- Review
- Targeting sorting nexin 3 to treat pulmonary fibrosis by dual modulating Wnt/β-catenin signaling.Cell death & disease · 2026Article
- Nanocarrier-Enabled siRNA Therapy for Pulmonary Fibrosis: Pharmacological Rationale, Delivery Barriers, and Translational Opportunities.International journal of nanomedicine · 2026Review
- Advances in Inhaled Nanoparticle Drug Delivery for Pulmonary Disease Management.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Tumor Microenvironment-Responsive Nanomedicines for Potentiating Cancer Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- SLC25A39 overexpression exacerbates lung adenocarcinoma progression and is negatively regulated by AFG3L2.NPJ precision oncology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary fibrosis (PF) is a life-threatening interstitial lung disease, characterized by excessive fibroblast activation and collagen deposition, leading to progressive pulmonary function decline and limited therapeutic efficacy. Here, the inhalable, myofibroblast-targeted, and pH-responsive liposomes (FL-NI) were developed for effective codelivery of nintedanib, a mainstream antifibrotic drug in clinic, and siIL11, a small interfering RNA that silences the key profibrosis cytokine IL-11. Notably, FL-NI achieved a 117.8% increase in pulmonary drug delivery by noninvasive inhalation and a 71.5% increase in delivery specifically to fibroblast activation protein-positive myofibroblasts while reducing nonspecific immune cell and epithelial uptake by 29.8 and 55.8%, respectively. The accurate inhalation codelivery of nintedanib and siIL11 into myofibroblasts achieved synergistic effects, effectively enhanced myofibroblast deactivation, reduced pathological collagen deposition by 50.8%, and promoted epithelial tissue repair. FL-NI remodeled the aberrant immune microenvironment without inducing systemic toxicities. Therefore, this work demonstrated the notable potential for this pluripotent strategy for improving PF outcomes and its promising clinical translation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.