ReviewAAPS PharmSciTech2023
Pulmonary Fibrosis: Unveiling the Pathogenesis, Exploring Therapeutic Targets, and Advancements in Drug Delivery Strategies.
Review in AAPS PharmSciTech, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 14 citations in OpenAlex.
- Development and Systematic Evaluation of a Low-Irritation PFD-AIS Formulation for Pulmonary-Targeted Therapy.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Oxymatrine attenuates pulmonary fibrosis via APE1‑mediated regulation of the PINK1/Parkin pathway.Molecular medicine reports · 2025Article
- Pirfenidone in Skin Fibrosis and Scarring: From Bench Insights to Clinical Data.Medical sciences (Basel, Switzerland) · 2025Review
- Identification and validation of CDC20 and ITCH as ubiquitination related biomarker in idiopathic pulmonary fibrosis.Hereditas · 2025Article
- GLP-1R activation attenuates the progression of pulmonary fibrosis via disrupting NLRP3 inflammasome/PFKFB3-driven glycolysis interaction and histone lactylation.Journal of translational medicine · 2024Article
- NLRP3 inflammasome mediates abnormal epithelial regeneration and distal lung remodeling in silica‑induced lung fibrosis.International journal of molecular medicine · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is an ailment with no cure and a very high rate of progression that ultimately leads to death. The exact reason for this disease is still not acknowledged. Many underlying mechanisms of wound healing and various types of stimuli that trigger the pathogenesis of IPF continue to be intensively explored. The exact therapy for the reversal of this disease is not yet known and is constantly in progress. Existing treatments only slow down the process or mitigate the symptoms to enhance the patient's healthcare system. The only two Food and Drug Administration-approved oral medications include pirfenidone and nintedanib whose high dose and systemic circulation can have side effects to a greater extent. Further research on restorative and extra-curative therapies for IPF is necessary due to the absence of viable therapeutic choices. To assure minimum off-targeted site delivery and longer duration of action, techniques that offer a sustainable release of the drug, better bioavailability, and patient compliance can be used.The work is an overview of the main therapeutic targets and pertinent developing therapies for the management of IPF. This study is an attempt to focus on various drug delivery systems that are responsible for showing effectiveness in defense mechanisms against IPF.
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.