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Fibrosis Resource Hub

Our comprehensive resource hub for preclinical fibrosis research is designed to support researchers by offering an extensive collection of tools, data, and literature specific to various pulmonary fibrosis (PF) models. Whether you are exploring the pathophysiology of the disease, evaluating potential therapeutics, or seeking detailed methodologies, our resources can be easily filtered to match your specific fibrosis model.

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Bleomycin-Induced PF l Silica-Induced PF l Radiation-Induced PF l Hydrochloric Acid Induced PF l Micro-CT Imaging

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Complete Lung Function Phenotyping (Resistance, Compliance, Lung Volume, PV Loops, FEV/FVC)

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WEBINAR SUMMARY —Developing Reproducible Small Animal Models to Better Reflect Lung Fibrosis Pathophysiology

The flexiVent & Fibrosis

Small Animal Models Of Pulmonary Fibrosis

Recent publications using the flexiVent to characterize lung function phenotypes in preclinical models of bleomycin-induced PF

Plausible role of INPP4A dysregulation in idiopathic pulmonary fibrosis. (2024). Arvind, M., et al. Physiological Reports, 12(9), e16302

INPP4A expression is altered in idiopathic pulmonary fibrosis (IPF), with upregulation observed in whole lung samples but downregulation in fibrotic regions. The expression levels of INPP4A are higher in the early stages of IPF compared to controls and negatively correlate with lung function indices, such as FVC and DLCO. However, treatment with an anti-INPP4A antibody worsened the condition in a mouse model, suggesting a complex, stage-dependent regulation of INPP4A in IPF.

Overexpression of Il-6 in Bleomycin-Treated Balb/C Mice Provides a New Model of Lung Fibrosis: Transcriptomic Comparison to Human Ipf. (2024). Richards, C., et al. Pulmonary and Respiratory Medicine, doi: 10.20944/preprints202407.2361.v1

A novel model of idiopathic pulmonary fibrosis (IPF) in BALB/c mice, combining transient overexpression of IL-6 with Bleomycin (AdIL-6+Bleo), has been developed and characterized. This model showed robust and sustained fibrosis, a unique cytokine profile, and increased activated T cells and macrophages, closely mimicking human IPF more accurately than existing rodent models. T cell depletion significantly reduced fibrotic responses, and the transcriptomic signature of this model shared more similarities with human IPF datasets, highlighting its potential for studying IPF mechanisms and therapeutic interventions.

Sinomenine ameliorates bleomycin-induced pulmonary fibrosis by inhibiting the differentiation of fibroblast into myofibroblast. (2024). Nie, Z., et al. Heliyon, 10(13). E33314

Sinomenine (SIN) demonstrated significant anti-pulmonary fibrosis properties in a bleomycin-induced mouse model and in TGF-β1-induced primary lung fibroblasts. The treatment reduced extracellular matrix deposition, hydroxyproline content, and improved lung function by inhibiting fibroblast-to-myofibroblast differentiation through suppression of aerobic glycolysis and Pfkfb3 expression. These findings highlight SIN’s potential as a promising therapeutic agent for pulmonary fibrosis by modulating metabolic pathways in fibroblasts.

Unraveling the mechanism of ethyl acetate extract from Prismatomeris connata Y. Z. Ruan root in treating pulmonary fibrosis: insights from bioinformatics, network pharmacology, and experimental validation. (2024). Li, S., et al. Frontiers in Immunology, 14, https://doi.org/10.3389/fimmu.2023.1330055

Through bioinformatics and experimental studies, we confirmed the pivotal role of macrophage polarization in idiopathic pulmonary fibrosis (IPF), identifying an imbalance in M1/M2 polarization with high expression of M2-associated biomarkers. Experiments demonstrated that the ethyl acetate extract HG2 from Prismatomeris connata Y. Z. Ruan effectively modulated macrophage polarization and altered the TGF-β/Smad pathway, showing therapeutic potential against bleomycin-induced pulmonary fibrosis. These findings suggest HG2 as a promising traditional Chinese medicine component for treating pulmonary fibrosis.

Nintedanib solid lipid nanoparticles improve oral bioavailability and ameliorate pulmonary fibrosis in vitro and in vivo models. (2024). International journal of Pharmaceutics, 649(5), 123644

Nintedanib-loaded solid lipid nanoparticles (NIN-SLN) were developed using a double-emulsification method to improve oral bioavailability and therapeutic efficacy against idiopathic pulmonary fibrosis (IPF). NIN-SLN treatment significantly downregulated fibrotic gene expression in diseased fibroblasts, showed a 2.87-fold increase in oral bioavailability, and improved lung tissue NIN levels compared to free NIN. In a bleomycin-induced IPF rat model, NIN-SLN attenuated lung fibrosis, improved lung function, and reduced gastrointestinal side effects, highlighting its potential as a superior treatment option for pulmonary fibrosis.

SGK1 aggravates idiopathic pulmonary fibrosis by triggering H3k27ac-mediated macrophage reprogramming and disturbing immune homeostasis. (2024). Wu, J., et al. International Journal of Biological Sciences, 20(3): 968-986

In idiopathic pulmonary fibrosis (IPF), increased SGK1-positive and M2-type macrophages were found in fibrotic areas, suggesting their role in disease progression. In a bleomycin and LPS-induced IPF mouse model, high SGK1 expression correlated with lung structure damage, increased fibrosis markers, and a disturbed immune environment. SGK1 promoted M2 macrophage reprogramming and subsequent immune disruption through GSK3β-TIP60-H3K27ac signaling, attracting Th17 cells and delivering TGF-β to fibroblasts, with these effects largely reversed by macrophage depletion, highlighting SGK1 as a potential therapeutic target.

Loss of ZNF451 mediates fibroblast activation and promotes lung fibrosis. (2024). Peng, H., et al. Respiratory Research 25(160)

In pulmonary fibrosis (PF), ZNF451 is downregulated and negatively correlated with disease severity. ZNF451 knockout mice exhibited more severe PF changes compared to wild-type mice, while overexpression of ZNF451 protected against bleomycin-induced fibrosis. Mechanistically, ZNF451 downregulation triggers fibroblast activation by increasing PDGFB expression and activating PI3K/Akt signaling, suggesting that ZNF451 could be a promising therapeutic target for PF.

Geneticin ameliorates pulmonary fibrosis by attenuating the TGF-β/Smad via modulating AMPK/SIRT1 signaling. (2024). Tirunavalli, S.K., & Andugulapati, S.B., et al. Life Sciences, 346, 122626

Geneticin demonstrated significant anti-fibrotic activity in both in vitro TGF-β-mediated differentiation models and an in vivo bleomycin-induced pulmonary fibrosis model. Treatment with geneticin reduced fibrotic markers, inflammatory cell infiltration, alveolar wall thickness, and collagen deposition, while improving lung structure and survival rates in a dose-dependent manner. Mechanistically, geneticin attenuated fibrosis by modulating the TGF-β/Smad and AMPK/SIRT1 signaling pathways, indicating its potential as a therapeutic agent for pulmonary fibrosis.

YAP1 inhibits the senescence of alveolar epithelial cells by targeting Prdx3 to alleviate pulmonary fibrosis. (2024). Su, W., et al. Experimental & Molecular Medicine, 56, 1643-1654

YAP1 expression is downregulated in alveolar type II (AT2) cells of idiopathic pulmonary fibrosis (IPF) patients, contributing to lung injury and impaired repair. Deletion of YAP1 in AT2 cells worsened lung injury and fibrosis, while its overexpression promoted alveolar regeneration, reduced fibrosis, and improved lung function by mitigating senescence and improving mitochondrial function via upregulation of Prdx3. This study suggests that YAP1 alleviates lung injury and fibrosis through Prdx3, presenting a potential novel therapeutic strategy for pulmonary fibrosis.

A WNT mimetic with broad spectrum FZD-specificity decreases fibrosis and improves function in a pulmonary damage model. (2024). Patel, M., et al., 25 (153)

A WNT mimetic agonist with broad FZD-binding specificity significantly expanded alveolar organoids and improved lung function in a bleomycin-induced pulmonary fibrosis model by decreasing inflammation and fibrosis. This therapeutic approach impacted multiple lung cell types in vivo, demonstrating its potential for tissue repair after lung damage. These findings support further development of Wnt/β-catenin pathway modulation as a regenerative therapy for pulmonary fibrosis.

Repetitive invasive lung function maneuvers do not accentuate experimental fibrosis in mice. (2024). Ropke, T., et al. Scientific Reports, 14: 13774

Repetitive lung function maneuvers using the FlexiVent system were well tolerated in mice and did not exacerbate experimental lung fibrosis induced by AdTGF-β1. This approach allows for monitoring the disease process within the same individual, reducing the number of animals required for longitudinal studies. The findings support the feasibility of repetitive lung function testing in mice, aligning with the 3R principle to reduce animal use in biomedical research.

Lung Cell Transplantation In Lung Fibrosis Treatment

WEBINAR SUMMARY —Developing Reproducible Small Animal Models to Better Reflect Lung Fibrosis Pathophysiology

FEV Measurements in Preclinical Models of Respiratory Disease

Small Animal Models Of Pulmonary Fibrosis

Recent publications using the flexiVent to characterize lung function phenotypes in preclinical models of silica-induced PF

Pulmonary osteoclast-like cells in silica induced pulmonary fibrosis. (2024). Hasegawa, Y., et al. Science Advances, 10(28)ary fibrosis. (2024). Arvind, M., et al. Physiological Reports, 12(9), e16302

In both human lung samples and a mouse model, silica exposure caused pulmonary inflammation and fibrosis, along with the differentiation of alveolar macrophages into osteoclast-like cells due to the RANKL cytokine. This osteoclast-like differentiation was found to contribute to progressive lung injury by releasing bone-resorbing proteases and hydrochloric acid. Treatment with anti-RANKL monoclonal antibodies successfully suppressed this differentiation and reduced lung fibrosis, highlighting a potential therapeutic approach for silicosis.

Bicyclol attenuates pulmonary fibrosis with silicosis via both canonical and non-canonical TGF-β1 signaling pathways. (2024). Tong-Tong, L., et al. Journal of Translational Medicine, 22(682)

Bicyclol (BIC) significantly improved lung function and reduced fibrosis progression in a rat model of silicosis by lowering inflammatory cell infiltration, cytokine levels, and collagen deposition. The underlying mechanisms involved BIC’s suppression of macrophage activation, polarization, and apoptosis, as well as inhibition of fibroblast-myofibroblast transition (FMT) and epithelial-mesenchymal transition (EMT) through targeting TGF-β1 pathways. These findings highlight BIC’s potential as a novel therapeutic agent for silicosis by preventing aberrant collagen deposition and slowing disease progression.

Inhibition of macrophage pyroptosis ameliorates silica-induced pulmonary fibrosis. (2023). Jiang, F., et al. Ecotoxicology and Environmental Safety, 268, 115693

This study investigated the role of macrophage pyroptosis in silica-induced pulmonary fibrosis using a mouse model and in vitro experiments. Silica exposure upregulated pyroptosis-related indicators, including GSDMD, in macrophages, and this induced macrophage pyroptosis promoted the activation of fibroblasts and fibrosis markers. Inhibiting GSDMD and macrophage pyroptosis suppressed these effects, suggesting that targeting macrophage pyroptosis could be a viable strategy to mitigate silicosis.

Differential pulmonary toxicity and autoantibody formation in genetically distinct mouse strains following combined exposure to silica and diesel exhaust particles. (2024). Janssen, L.M.F., et al. Particle and Fibre Toxicology, 21(8).

This study assessed the effects of silica and diesel exhaust particles (DEP) on lung injury, inflammation, and autoantibody formation in two mouse strains, C57BL/6J and NOD/ShiLtJ. Silica exposure caused significant inflammatory responses, cytokine release, and mild fibrosis in both strains, with NOD/ShiLtJ mice showing pronounced airway hyperreactivity and higher antinuclear antibody levels. Despite DEP-loaded macrophages and particle co-localization, ambient-level DEP did not significantly enhance silica-induced lung damage or inflammation, indicating minimal additional impact from DEP exposure in these mouse strains.

Human umbilical cord mesenchymal stem cell-derived extracellular vesicles alleviated silica induced lung inflammation and fibrosis in mice via circPWWP2A/miR-223–3p/NLRP3 axis. (2023). Hou, L., et al. Ecotoxicology and Environmental Safety, 251, 114537

This study highlights the potential of human umbilical cord mesenchymal stem cell-derived extracellular vesicles (hucMSC-EVs) as a treatment for silicosis by leveraging the circPWWP2A/miR-223–3p/NLRP3 axis. The results showed that miR-223–3p, delivered by hucMSC-EVs, decreased inflammation and fibrosis by targeting NLRP3, which was otherwise suppressed by circPWWP2A after silica exposure. This mechanism was shown to alleviate silica-induced lung injury and inflammation, suggesting a novel therapeutic strategy for silicosis.

Combined therapy with pirfenidone and nintedanib counteracts fibrotic silicosis in mice. (2023). Bai, L., et al. Authorea, DOI: 10.22541/au.169779616.60916387/v1

This study assessed the efficacy of pirfenidone and nintedanib, alone and in combination, in treating advanced silicosis in mouse models. The results demonstrated that both drugs were effective, with combination therapy yielding superior outcomes by modulating immune responses, signaling pathways, circadian rhythms, and various metabolic processes. The findings suggest that combined therapy, even at lower doses, offers significant therapeutic potential for advanced silicosis through diverse biological mechanisms.

MiR-26a-5p from HucMSC-derived extracellular vesicles inhibits epithelial mesenchymal transition by targeting Adam17 in silica-induced lung fibrosis. (2023). Zhao, J., et al. Ecotoxicology and Environmental Safety, 257, 114950

This study demonstrated that human umbilical cord mesenchymal stem cell-derived extracellular vesicles (hucMSC-EVs) can serve as a potential therapeutic carrier in silicosis by inhibiting epithelial-mesenchymal transition (EMT) in silica-induced lung fibrosis. The hucMSC-EVs, enriched with miR-26a-5p, suppressed EMT by targeting and inhibiting the Adam17/Notch signaling pathway. These findings suggest that hucMSC-EVs could provide a novel therapeutic approach for treating silicosis fibrosis.

Lung Cell Transplantation In Lung Fibrosis Treatment

WEBINAR SUMMARY —Developing Reproducible Small Animal Models to Better Reflect Lung Fibrosis Pathophysiology

Longitudinal Micro‑CT Derived Biomarkers in Silicosis Fibrosis Model

The flexiVent & Fibrosis

Recent publications using the flexiVent to characterize lung function phenotypes in preclinical models of radiation-induced PF

Development of a Radiation-induced Pulmonary Fibrosis Partial Body Irradiation Model in C57BL/6 Mice. (2024). Kumar, V.P., et al. Radiation Research, 201(5): 460-470

A murine model for partial-body irradiation (PBI) with 2.5% bone marrow sparing (BM2.5–PBI) was used to study long-term lung damage from radiation exposure. Six to seven months post-irradiation, µ-CT scans revealed pulmonary fibrosis characterized by ground glass opacity, stiffer lung tissue, and reduced inspiratory capacity. Histopathological and molecular analyses confirmed the presence of fibrotic lesions and elevated pro-fibrotic biomarkers, establishing this model as a valuable tool for testing countermeasures against radiation-induced pulmonary fibrosis.

Th17 Cells Mediate Senescence in Radiation-induced Pulmonary Fibrosis (RIPF) Murine Model (2024). Am J Respir Crit Care Med 2024;209:A2496

The study investigated the role of the Th17/IL-17A pathway in radiation-induced pulmonary fibrosis (RIPF) in mice. Results showed that radiation increased cellular senescence and the expression of senescence-associated markers (SA-β-Gal, p53, IL-6, IL-8, PAI-1, IL-1β, TNF-α) and pro-inflammatory factors (TGFβ-1, IL-17A) in lung tissues. Additionally, changes in fibrinolytic markers (uPA, uPAR) were linked to increased lung resistance and elastance, suggesting a potential target for therapeutic intervention in RIPF.

Development of a Radiation-induced Pulmonary Fibrosis Partial Body Irradiation Model in C57BL/6 Mice. (2024). Kumar, V.P., et al. Radiation Research, 201(5): 460-470

A murine model for partial-body irradiation (PBI) with 2.5% bone marrow sparing (BM2.5–PBI) was used to study long-term lung damage from radiation exposure. Six to seven months post-irradiation, µ-CT scans revealed pulmonary fibrosis characterized by ground glass opacity, stiffer lung tissue, and reduced inspiratory capacity. Histopathological and molecular analyses confirmed the presence of fibrotic lesions and elevated pro-fibrotic biomarkers, establishing this model as a valuable tool for testing countermeasures against radiation-induced pulmonary fibrosis.

NXC736 Attenuates Radiation-Induced Lung Fibrosis via Regulating NLRP3/IL-1β Signaling Pathway. (2023). International Journal of Molecular Sciences, 24(22), 16265, https://doi.org/10.3390/ijms242216265

The study evaluated the effects of NXC736, a novel NLRP3 inhibitor, on radiation-induced lung fibrosis (RILF) in a mouse model. Results showed that NXC736 treatment reduced collagen deposition, inflammatory cell infiltration, and damaged lung volume, while also improving lung function. The compound inhibited the NLRP3 inflammasome activation and blocked the fibrotic pathway by reducing IL-1β expression and epithelial-mesenchymal transition markers, suggesting its potential as a therapeutic agent against RILF.

Efferocytosis and enhanced FPR2 expression following apoptotic cell instillation attenuate radiation-induced lung inflammation and fibrosis. (2022). Kim, S.Y., et al. Biochemical and Biophysical Research Communications, Volume 601, Pages 38-44

The study examined the impact of efferocytosis, induced by apoptotic cell instillation, on radiation-induced lung injury (RILI) in a mouse model. Results demonstrated that injecting apoptotic cells into the lungs increased FPR2 mRNA levels, reduced lung damage, and improved lung function following irradiation. The treatment also decreased the expression of inflammatory cytokines, fibrosis-related markers, and oxidative stress markers, indicating that enhanced FPR2 expression through efferocytosis alleviates lung inflammation and fibrosis.

WEBINAR SUMMARY —Developing Reproducible Small Animal Models to Better Reflect Lung Fibrosis Pathophysiology

Longitudinal Micro‑CT Derived Biomarkers in Silicosis Fibrosis Model

Recent publications using the flexiVent to characterize lung function phenotypes in preclinical models of Hcl-induced PF

HSP70 Is a Critical Regulator of HSP90 Inhibitor’s Effectiveness in Preventing HCl-Induced Chronic Lung Injury and Pulmonary Fibrosis. (2024). Colunga Biancatelli, R.M. et al, International journal of Molecular Sciences, 25(3): 1920 https://doi.org/10.3390/ijms25031920

Exposure to hydrochloric acid (HCl) can lead to acute and chronic lung injury, with no FDA-approved treatments available. In this study, the HSP70 inducer geranylgeranyl-acetone (GGA) improved HCl-induced lung microvascular endothelial cell barrier dysfunction and, when combined with the HSP90 inhibitor TAS-116, further enhanced its protective effects against chronic lung injury in mice. Conversely, the HSP70 suppressant gefitinib (GFT) exacerbated HCl-induced injury and impaired TAS-116’s protective effects, suggesting that combined treatment with HSP90 inhibitors and HSP70 inducers could be a novel therapeutic approach for HCl-induced lung injury and pulmonary fibrosis.

Combined Treatment With HSP90 Inhibitors and HSP70 Inducers Ameliorates HCl-induced Chronic Lung Injury and Pulmonary Fibrosis in New Zealand White Rabbits. (2024). Colunga Biancatelli, R.M. et al, ATS Journals, A105

Inhalation of hydrochloric acid (HCl) leads to significant acute and chronic lung injury, with HSP90 identified as a potential therapeutic target. In a study with New Zealand white rabbits, HSP90 inhibitor TAS-116, alone or combined with HSP70 inducer GGA, was found to reduce alveolar inflammation, lung dysfunction, and fibrosis caused by HCl exposure, with the combination treatment showing the most significant improvement in lung function. These findings suggest that combined HSP90 and HSP70 modulation could be a promising therapeutic approach for treating HCl-induced pulmonary fibrosis, supporting further clinical research.

The Heat Shock Protein 90 Inhibitor, AT13387, Protects the Alveolo-Capillary Barrier and Prevents HCl-Induced Chronic Lung Injury and Pulmonary Fibrosis. (2022). Colunga Biancatelli, R.M.L., et al. Cells, 2022, 11(6): 1046, https://doi.org/10.3390/cells11061046

Hydrochloric acid (HCl) exposure leads to persistent alveolar inflammation, fibrosis, and lung function decline, mimicking conditions like asthma and reactive airways dysfunction syndrome. The HSP90 inhibitor AT13387, administered subcutaneously, significantly reduced alveolar inflammation, fibrosis, and hyperresponsiveness to methacholine in HCl-exposed mice, while also blocking key profibrotic pathways and restoring barrier function in vitro. These findings suggest that AT13387 is a promising candidate for treating chronic lung injury induced by HCl, highlighting its potential for clinical use at low, non-toxic doses.

Small Animal Models Of Pulmonary Fibrosis

Recent publications using the flexiVent to characterize lung function phenotypes and sync with microCT imaging in preclinical models of PF

Multiphase micro-computed tomography reconstructions provide dynamic respiratory function in a mouse lung fibrosis model. (2024). Pennati, F., et al. iScience, 27(3), 109262

Using bleomycin-induced lung fibrosis and the antifibrotic drug nintedanib as models, a novel four-dimensional (4D) micro-CT imaging approach was developed to visualize lung dynamics across a full respiratory cycle. This method, which includes 30 reconstructed volumes per cycle and deep-learning-assisted segmentation, accurately described inhalatory and exhalatory lung dynamics, revealing an obstructive pattern at day 7 and a restrictive pattern due to fibrosis at day 21. Nintedanib treatment resulted in milder restriction and fibrotic pathology, demonstrating the potential of 4D micro-CT as a powerful tool for discovering clinically relevant therapeutic compounds.

Longitudinal Micro-Computed Tomography Detects Onset and Progression of Pulmonary Fibrosis in Conditional Nedd4-2 Deficient Mice. (2024). Leitz, D.H.W., et al. bioRxiv, doi: https://doi.org/10.1101/2023.08.31.555725

In this study, longitudinal micro-CT imaging was used to monitor the onset and progression of IPF-like lung disease in conditional Nedd4-2−/− mice. The findings revealed that micro-CT could detect nonspecific interstitial alterations at 3 months and key IPF-like features, such as honeycombing lesions, from 4 months onwards. Additionally, a strong inverse correlation was observed between pulmonary function and micro-CT fibrosis scores, highlighting micro-CT’s sensitivity as a quantitative endpoint for preclinical antifibrotic strategy evaluation.

Application-specific approaches to MicroCT for evaluation of mouse models of pulmonary disease. (2023). Redente, E.F., et al. PLOS One, https://doi.org/10.1371/journal.pone.0281452

This study introduces an automated pulmonary air and tissue segmentation (PATS) task list to enhance the efficiency and reduce user bias in micro-CT image analysis of lung health and disease in small animal models. The PATS task list was validated using four distinct imaging methods, including in vivo respiration-controlled scanning and ex vivo high-resolution scanning, and showed effective segmentation compared to manual analysis. This automated approach demonstrates significant improvements in the standardization and efficiency of preclinical micro-CT imaging and analysis across various lung disease models.

Microcomputed tomography visualization and quantitation of the pulmonary arterial microvascular tree in mouse models of chronic lung disease. (2023). Schneider, B., et al. Pulmonary Circulation, 13(3): e12279

This study developed a novel method using microcomputed tomography (µCT) imaging to visualize and quantify the murine pulmonary arterial circulation, enabling detailed examination of microvessels down to approximately 6 µM in diameter. The method was validated by demonstrating significant alterations in arterial vessel structure in three-dimensional models following bleomycin-induced injury at peak fibrosis. This advanced perfusion and analysis technique facilitates the detailed study of pulmonary vascular remodeling and angiogenesis in chronic lung diseases and post-injury repair.

Microscopic computed tomography with AI-CNN-powered image analysis: the path to phenotype bleomycin-induced lung injury. (2024). Henneke, I., et al. American Journal of Physiology, 326(6): C1637-C1647

This study demonstrated the utility of microscopic computed tomography (µCT) combined with AI-CNN-powered lung segmentation for rapid and accurate phenotyping of bleomycin-induced lung injury in mice. The µCT imaging revealed time-dependent development of lung injury, with significant changes in lung density, air-to-tissue volume ratio, and lung aeration, which correlated well with invasive lung function measurements and histological collagen content. This method provides a powerful tool for noninvasive monitoring of disease progression and therapeutic effects, enhancing the efficiency and reliability of preclinical studies.

Longitudinal Micro‑CT Derived Biomarkers in Silicosis Fibrosis Model

Small Animal Models Of Pulmonary Fibrosis

Protocols

Download our protocol describing the procedures required to perform forced-oscillation measurements of respiratory mechanics in mice at baseline and following increasing aerosolized methacholine challenges, using the flexiVent.

Learn the steps and procedures required to adequately perform a bronchoalveolar lavage (BAL) following measurements of respiratory mechanics in mice using the flexiVent systems in our BAL protocol document.

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Fibrosis Resource Hub

Filter by model:

Bleomycin-Induced PF l Silica-Induced PF l Radiation-Induced PF l Hydrochloric Acid Induced PF l Micro-CT Imaging

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Quick Resources

Bleomycin-Induced PF

Recent publications using the flexiVent to characterize lung function phenotypes in preclinical models of bleomycin-induced PF

Silica-Induced Pulmonary Fibrosis

Recent publications using the flexiVent to characterize lung function phenotypes in preclinical models of silica-induced PF

Radiation-Induced Pulmonary Fibrosis

Recent publications using the flexiVent to characterize lung function phenotypes in preclinical models of radiation-induced PF

Hydrochloric Acid Induced Pulmonary Fibrosis

Recent publications using the flexiVent to characterize lung function phenotypes in preclinical models of Hcl-induced PF

Micro-CT Imaging

Recent publications using the flexiVent to characterize lung function phenotypes and sync with microCT imaging in preclinical models of PF

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Protocols

Request a Free Custom Literature Search