Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis

Genome-wide analysis of tandem repeat variation identifies SLC15A4 as a susceptibility gene for idiopathic pulmonary fibrosis

This study identifies SLC15A4 as a susceptibility gene for IPF through genome-wide analysis of tandem repeat variation, showing its role in gene expression and disease risk.

Ferret model of bleomycin-induced lung injury shares features of human idiopathic pulmonary fibrosis

This study shows that a bleomycin-induced lung injury model in ferrets shares key pathophysiological, cellular, and molecular features with human idiopathic pulmonary fibrosis, suggesting its use for IPF research.

Spatio-Temporal Multi-Omics Profiling of Mechanisms and Biomarkers in Inhaled Drug-Induced Lung Toxicity

This study develops a multi-omics framework to identify biomarkers of inhaled drug-induced lung toxicity using spatial transcriptomics, proteomics, and histopathological data.

T-cell Multiomic Analysis Identifies Subsets and Mechanisms of Interaction with Epithelial Cells in Idiopathic Pulmonary Fibrosis

The paper identifies T-cell subsets and their interactions with epithelial cells in IPF using multiomic profiling, revealing novel signaling pathways and activation patterns.

Tankyrase inhibition demonstrates anti-fibrotic effects in preclinical pulmonary fibrosis models

This study shows that the TNKS inhibitor OM-153 reduces fibrosis markers and ECM expression in multiple preclinical IPF models by inhibiting WNT/β-catenin and YAP signaling.

An aerosolised dual-action Autotaxin inhibitor- PPARγ agonist for the treatment of pulmonary fibrosis

This paper introduces EL244, a dual ATX inhibitor and PPARγ agonist for treating pulmonary fibrosis, showing reduced LPA levels and fibrosis in a bleomycin model.

Curated and harmonised transcriptomics datasets of interstitial lung diseases

This paper curates and harmonizes transcriptomics datasets from interstitial lung disease patients to improve data FAIRness and enable integrated systems biology approaches.

Loss of tight junction protein claudin 18 uncovers alveolar epithelial stem cell plasticity and emergence of non-fibrogenic transitional progenitors

The paper identifies regeneration-associated transitional progenitors (RATPs) in Cldn18 knockout mice, showing they are less fibrogenic and contribute to lung repair rather than fibrosis.

Modeling Endothelial Dysfunction in Idiopathic Pulmonary Fibrosis: Bridging Mechanistic Insights and Translational Applications

This paper identifies PMVEC alterations in IPF using single-cell RNA sequencing and spatial transcriptomics, develops endothelial injury models, and validates functional assays for drug discovery.

Spatial and Single-cell Transcriptomics Reveal Programs Governing Fibroblastic Foci Fibroblasts

The paper identifies transcriptional programs in fibroblastic foci fibroblasts using spatial and single-cell transcriptomics, revealing MMP11 as a prognostic biomarker and potential therapeutic target.

Phosphatidylcholine Metabolism Controls Alveolar Progenitor Renewal and Pulmonary Fibrosis

This study identifies LPCAT1 as a critical regulator of AT2 cell renewal and lipid metabolism in IPF, showing that reactivating LPCAT1 can mitigate lung fibrosis.

Monocyte Subset Predict Clinical Outcomes in Fibrotic Hypersensitivity Pneumonitis

The paper identifies monocyte subsets associated with clinical outcomes in fibrotic hypersensitivity pneumonitis using single-cell RNA sequencing.

Bispecific Targeting of CHI3L1 and PD-1/PD-L1 Axis as a Novel Therapeutic Strategy for Idiopathic Pulmonary Fibrosis

This study identifies a stimulatory interaction between CHI3L1 and the PD-1/PD-L1 axis in pulmonary fibrosis and shows that bispecific targeting of both reduces fibrosis in mice.

Loss of Regulator of telomere elongation helicase (Rtel1) impairs alveolar epithelial cell progenitor function but does not exacerbate experimental fibrosis

This study shows RTEL1 regulates alveolar epithelial cell progenitor function but does not worsen experimental lung fibrosis in mice.

Bigh3 is essential for pulmonary fibrosis

This study shows Bigh3 is essential for lung fibrosis by demonstrating its role in fibroblast-macrophage interactions and collagen expression.

Pre-clinical proof-of-concept of anti-fibrotic activity of caveolin-1 scaffolding domain peptide LTI-03 in ex vivo precision cut lung slices from patients with Idiopathic Pulmonary Fibrosis

This study evaluates the anti-fibrotic effects of LTI-03 in IPF patient-derived precision cut lung slices, showing dose-dependent reduction of fibrotic markers.

AI-Driven Toolset for IPF and Aging Research Associates Lung Fibrosis with Accelerated Aging

The paper develops an AI-driven toolset to study IPF and aging, showing IPF as a dysregulation of aging processes rather than just accelerated aging.

Siglec-F Deficiency Prevents Fibrosis After Bleomycin-Induced Acute Lung Injury

This study shows that Siglec-F deficiency reduces fibrosis in bleomycin-induced lung injury by altering gene expression in airspace macrophages.

A Simultaneous Inhibition of ID1 and ID3 Protects Against Pulmonary Fibrosis

This study shows that inhibiting both ID1 and ID3 reduces pulmonary fibrosis in mice and human cells by blocking fibroblast proliferation and differentiation.

Endogenous gene editing of alveolar organoids reveals that expression of pathogenic variant SFTPC-I73T disrupts endosomal function, epithelial polarity and wound healing

The Old genetically heterogeneous Mouse Model Recapitulates Chronic and Persistent Idiopathic Pulmonary Fibrosis with Strong Senescence Signatures

This study develops an improved IPF mouse model using aged mice that better mimics the persistent disease features and senescence observed in humans.

Pharmacological Inhibition of Epac1 Protects against Pulmonary Fibrosis by Blocking FoxO3a Neddylation

This study shows that inhibiting Epac1 with AM-001 reduces fibroblast proliferation and profibrotic markers, protecting against pulmonary fibrosis in mouse models and human lung slices.

Macropinocytosis inhibition attenuates pro-fibrotic responses in lung fibroblasts and pulmonary fibrosis

This study shows that inhibiting macropinocytosis reduces fibrotic responses in lung fibroblasts and ameliorates pulmonary fibrosis in mice.

AHR activation accelerates the resolution of TGF-β1 induced fibroblast activation and promotes alveolar type 1 cell regeneration in alveolar organoids

The paper identifies DB-11-BE87 as a compound that promotes AT1 cell regeneration by reducing TGF-β1-induced fibroblast activation through AHR activation in alveolar organoids.

Endothelial Sensitivity to Pro-Fibrotic Signals Links Systemic exposure to Pulmonary Fibrosis

This study shows that endothelial cells are sensitive to systemic pro-fibrotic signals and initiate early pro-fibrotic mechanisms in pulmonary fibrosis, independent of other cell types.

Impaired AMPK Control of Alveolar Epithelial Cell Metabolism Promotes Pulmonary Fibrosis

The paper identifies impaired AMPK signaling in AT2 cells as a driver of pulmonary fibrosis and shows restoring AMPK alleviates fibrosis in vivo.

Activation of the impaired NAMPT/SIRT7/SOD2 axis restores alveolar progenitor cell homeostasis in idiopathic pulmonary fibrosis and reverses pulmonary fibrosis in mice

This study identifies NAMPT as a key regulator of alveolar progenitor cell function in IPF, showing that its activation restores homeostasis and reverses fibrosis in mice.

PTX3 Governs Fibroblast-Epithelial Dynamics in Lung Injury and Repair

This study identifies PTX3 as a key antifibrotic factor secreted by fibroblasts that modulates epithelial repair in acute injury and exacerbates damage in chronic injury.

YAP/TAZ activation in fibroblasts coordinates fibrotic remodeling, fibroinflammation, and epithelial dysfunction in pulmonary fibrosis

This study shows YAP/TAZ activation in fibroblasts drives fibrosis, fibroinflammation, and epithelial dysfunction in pulmonary fibrosis, with potential therapeutic targeting.

The MUC5B promoter variant results in proteomic changes in the non-fibrotic lung

This study identifies proteomic changes in non-fibrotic lung tissue associated with the MUC5B promoter variant, linking them to fibrosis progression.