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Open research questions in Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis

217 unresolved questions extracted from the limitations and future-work sections of 461 Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis papers in our library. Each links back to the study that raised it.

What the literature leaves open

  • Immortal time bias in the analysis of anthracycline exposure. Potential small-sample bias and sparse event limitations in the estimation of hazard ratios and confidence intervals. Limited temporal resolution in the exploratory cytokine profiling analysis.

    Spliceosome gene mutations synergize with anthracyclines to amplify atrial fibrillation risk in hematologic malignancies: a multicenter cohort study with discovery and validation · 2026 · DOI

  • Exploratory cytokine profiling indicates an inflammatory axis, but these analyses were limited and lack temporal resolution, - The study had a retrospective design, - The study lacked a control group without hematologic malignancies

    Spliceosome gene mutations synergize with anthracyclines to amplify atrial fibrillation risk in hematologic malignancies: a multicenter cohort study with discovery and validation · 2026 · DOI

  • Missing exposure or covariate data led to exclusions, - Participants with missing values for covariates with less than 5% missingness were excluded, - For covariates with more than 5% missing values, an 'unknown' category was created

    Smoking exposures and mortality risk in individuals with idiopathic pulmonary fibrosis: a UK Biobank cohort study · 2026 · DOI

  • Investigating life-course smoking exposure and joint mortality patterns with recorded IPF, - Examining cumulative smoking and its effects on mortality, - Studying the effects of smoking exposure on IPF prognosis

    Smoking exposures and mortality risk in individuals with idiopathic pulmonary fibrosis: a UK Biobank cohort study · 2026 · DOI

  • further studies are needed to investigate the mechanisms linking glycocalyx degradation to epithelial barrier injury, - the therapeutic potential of CV122 in human COPD patients should be explored, - the effects of CV122 on other respiratory diseases could be investigated

    Targeting heparanase-associated epithelial glycocalyx remodeling attenuates Akt/NF-κB–related barrier dysfunction in experimental COPD · 2026 · DOI

  • The mechanisms linking glycocalyx degradation to epithelial barrier injury in COPD are not well understood. Current therapies do not directly target glycocalyx degradation or HPSE activity.

    Targeting heparanase-associated epithelial glycocalyx remodeling attenuates Akt/NF-κB–related barrier dysfunction in experimental COPD · 2026 · DOI

  • Investigating the molecular basis of lipid peroxidation and ferroptosis in pulmonary fibrosis - Examining the effects of antifibrotic therapies on lipid metabolism and ferroptosis

    Lipid metabolism as a cell-state determinant in pulmonary fibrosis: from epithelial failure to ferroptosis-driven amplification · 2026 · DOI

  • The mechanisms underlying the progression of pulmonary fibrosis despite antifibrotic therapy. The role of lipid metabolism in determining cell-state stability in pulmonary fibrosis. The compartment-specific lipid metabolic programs that contribute to the profibrotic microenvironment.

    Lipid metabolism as a cell-state determinant in pulmonary fibrosis: from epithelial failure to ferroptosis-driven amplification · 2026 · DOI

  • further studies are needed to confirm the association between air pollution and IPF progression, - studies should investigate the effects of specific air pollutants on IPF, - research should focus on developing strategies to reduce air pollution exposure in patients with IPF, - longitudinal studies are needed to examine the long-term effects of air pollution on IPF

    Air pollution exposure and its effects on idiopathic pulmonary fibrosis: clinical worsening, lung function decline, and radiological deterioration · 2024 · DOI

  • Further studies are needed to understand the complex interactions between Notch and TGF-β signaling pathways - Research on the molecular mechanisms of these interactions is necessary to develop effective therapeutic strategies

    The Complex Interplay of TGF-β and Notch Signaling in the Pathogenesis of Fibrosis · 2024 · DOI

  • The complex interplay of genetic, epigenetic, and pathophysiological factors in IPF makes it challenging to develop effective treatments. Current therapeutic options are limited and non-curative. There is a need for new integrated endpoints in IPF research.

    Highlights on Future Treatments of IPF: Clues and Pitfalls · 2024 · DOI

  • Systematic characterisation of commercial reagents, - Open dissemination of results

    A guide to selecting high-performing antibodies for TGF-beta receptor type-2 (UniProt ID: P37173) for use in western blot and flow cytometry · 2026 · DOI

  • personalized medicine approaches, - artificial intelligence integration, - growth in genetic insights, - novel drug targets

    Highlights on Future Treatments of IPF: Clues and Pitfalls · 2024 · DOI

  • The relationship between sarcopenia and nintedanib treatment is not well understood. Prior studies have not fully explored the effect of sarcopenia on patients with interstitial lung disease.

    Sarcopenia affects the outcomes and tolerability in patients with interstitial lung disease receiving nintedanib: a retrospective study · 2026 · DOI

  • Post-COVID-19 residual lung abnormalities (RLA) are associated with persistent respiratory symptoms and radiological changes, yet the underlying mechanisms remain unclear.

    Multi-omics reveals a monocyte-macrophage-fibroblast axis in post-COVID-19 fibroinflammatory lung remodelling · 2026 · DOI

  • While the flavonol quercetin exhibits established anti-inflammatory and antioxidant properties, its therapeutic mechanisms against IPF—particularly regarding epithelial-mesenchymal transition (EMT) and inflammation regulation via the follistatin-like 1 (FSTL1)/nuclear factor kappa B (NF-κB) axis—remain incompletely elucidated.

    Quercetin ameliorates epithelial-mesenchymal transition and inflammation by targeting FSTL1 and modulating the NF-κB pathway in pulmonary fibrosis · 2025 · DOI

  • Background: Glycolysis plays a crucial role in fibrosis, but the specific genes involved in glycolysis in idiopathic pulmonary fibrosis (IPF) are not well understood.

    Identification of glycolysis-related gene signatures for prognosis and therapeutic targeting in idiopathic pulmonary fibrosis · 2025 · DOI

  • , unclear causal relationship, lack of standardized intervention protocols) and future research directions, providing a new framework for PF mechanism research and clinical intervention.

    Lung-gut axis, intestinal microbiota, and pulmonary fibrosis: mechanisms and therapeutic potential · 2025 · DOI

  • These results suggest that targeting TNIK with rentosertib is safe and well tolerated and warrants further investigation in larger-scale clinical trials of longer duration.

    A generative AI-discovered TNIK inhibitor for idiopathic pulmonary fibrosis: a randomized phase 2a trial · 2025 · DOI

  • Further research into RUNX could contribute to the development of novel therapeutic approaches for fibrosis.

    Runt-related transcription factors: from pathogenesis to therapeutic targets in multiple-organ fibrosis · 2025 · DOI

  • Enhancing the homing and retention of MSCs in lung tissue is critical for maximizing their therapeutic efficacy, yet an effective strategy for overcoming this challenge is still lacking.

    Targeted peptide modification of mesenchymal stem cells enhances their therapeutic efficacy in the treatment of idiopathic pulmonary fibrosis · 2025 · DOI

  • However, the pathogeny of IPF is poorly understood, and therapeutic options are very limited.

    Periodontitis aggravates pulmonary fibrosis by Porphyromonas gingivalis-promoted infiltration of neutrophils and Th17 cells · 2025 · DOI

  • These findings offer new insights for IPF treatment and further investigation of potential side effects.

    Genetic insights into idiopathic pulmonary fibrosis: a multi-omics approach to identify potential therapeutic targets · 2025 · DOI

  • BACKGROUND: Interstitial lung disease (ILD) is a common and severe comorbidity of rheumatoid arthritis (RA), yet reliable diagnostic biomarkers remain lacking.

    Identification EXOSC4 as a novel autoantigen of interstitial lung disease in rheumatoid arthritis · 2025 · DOI

  • It also discussed current issues and prospects, aiming to provide a reference for further research on the mechanism of PF, drug development, and clinical trials.

    A Chinese classical prescription Maimendong decoction in treatment of pulmonary fibrosis: an overview · 2024 · DOI

Most-cited papers in Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis

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217 open questions have been extracted from the limitations and future-work passages of 461 Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis papers in our library. Each one below links back to the study that raised it, so you can read the original claim in context.

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