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Pulmonary Fibrosis Explained: Causes, Treatments and New Research

September 29, 2026  |  Read time: 6 mins

Beth Wright

‍

Healthy lungs are soft and elastic.

With the help of your diaphragm and various muscle groups they are pulled open when you breathe in and spring back when you breathe out [1].

What happens when lung elasticity is gone?

Pulmonary fibrosis is a debilitating disease that takes that soft elasticity away, replacing it with inflexible scar tissue (fibrosis). This scar tissue builds up between the lungs' air sacs, making lungs stiffer and harder to expand. As a result, breathing takes more effort and less oxygen can cross from the lungs into the bloodstream [2].

Pulmonary fibrosis is the most common, and serious, form of end stage interstitial lung disease (ILD).

Unpacking Interstitial Lung Disease (ILD) and its relation to pulmonary fibrosis

ILD is not just one disorder. ILD is the umbrella term for conditions that damage the tissue supporting the lungs' air sacs [3].

For the curious readers, you would be right to wonder what exactly the interstitium is.

In medical terms the lung interstitium is the space between the tiny air sacs in your lungs (the alveoli) and the small blood vessels surrounding them. The interstitium is essential as the oxygen from your alveoli passes through it into your blood, and in the same breath carbon dioxide moves into your air sacs.

Alveoli cannot regrow and once they are damaged, they are gone for good. This alone goes to show just how dangerous diseases of this nature can be. Some ILDs include:

What happens inside a lung with fibrosis?

Fibrosis begins when the delicate cells lining the air sacs are repeatedly injured. Where in a healthy lung, injury triggers a tidy repair process. In fibrosis, repair does not go so smoothly.

The repeated injury damages the lining cells of the alveoli, and faulty repair recruits fibroblasts, the cells that lay down structural tissue. Those fibroblasts pump out extracellular matrix [4], a mesh of proteins including collagen that normally holds tissue in shape. Too much of it fills spaces that should stay open and flexible.

The lung is rebuilt incorrectly, and gas exchange becomes progressively less efficient.

‍

Outside the lung, the lack of oxygen causes havoc on the body, leading to symptoms like weight loss, cyanosis (blue-tinted skin), fatigue, and even clubbed fingers [5].

‍

Why does pulmonary fibrosis develop?

There is no single cause, which is part of why it is hard to treat.

Current thinking is that fibrosis develops when someone genetically susceptible is exposed to damaging environmental factors over a long period [5].

Hence, several layers interact: inherited genetic variants, epigenetic changes (chemical markers that switch genes on and off without altering DNA itself), ageing, long term exposure to inhaled irritants, and immune dysfunction that keeps inflammation running [5].

Interestingly, ageing plays a particularly telling role in fibrosis development [6-8].

Fibroblasts taken from fibrotic lungs look prematurely old. They show markers of cellular senescence, a state in which a cell stops dividing but refuses to die [9]. These lingering cells release inflammatory signals that drive further scarring in the tissue around them. Drugs designed to clear them, called 'senolytics', are one experimental avenue under investigation [10].

Historically, the irreversible damage has meant a poor outlook for idiopathic pulmonary fibrosis (IPF) has been poor with median survival after diagnosis roughly three to five years. However, this number came about before the use of antifibrotics became more common. It’s important to note that averages cannot predict any individual's course, but it can help to explain the urgency in this field.

Are there treatment options improving prognoses?

‍

Pulmonary fibrosis treatment options available today

Antifibrotic drugs: pirfenidone and nintedanib

Two antifibrotic medications are currently approved, but they work quite differently [1, 10].

Pirfenidone slows fibroblasts from multiplying and reduces collagen production, largely by dampening TGF beta, one of the master switches for scarring [11]. Side effects include gastrointestinal upset and skin sensitivity.

Nintedanib blocks specific molecular signals that tell cells to grow and move, interrupting fibroblast growth, migration and the extracellular matrix production [12]. Its side effects, however, tend to be more pronounced than Pirfenidone [11], particularly diarrhoea, nausea and vomiting.

Both slow the decline in lung function, which is genuinely valuable. Neither relieves symptoms, and neither reverses existing scarring.

Yet, reported discontinuation rates sit between 10 and 20%, meaning a meaningful proportion of people stop taking the medication designed to help them [13]. That gap between what a drug does on a lung function chart and what a person feels day to day is the strongest argument for better options.

Supportive treatments for pulmonary fibrosis

Care may also include supplemental oxygen therapy to reduce breathlessness, pulmonary rehabilitation (a structured program of exercise training, breathing techniques and education), and lung transplantation in advanced disease.

Oxygen therapy delivers additional oxygen to your bloodstream when the lung scarring makes it hard for your body to get enough on its own.

Earlier detection matters in pulmonary fibrosis

Every strategy described here works better the earlier it is applied. Preventing scar tissue from forming is a far more tractable problem than dismantling it once set.

Yet, pulmonary fibrosis is frequently caught late [14]. Early symptoms, including breathlessness on exertion and a persistent dry cough, are easily attributed to ageing or a lingering infection. By the time imaging shows characteristic changes, meaningful lung tissue has often already been lost.

Closing that gap is one of the most valuable things respiratory medicine can do.

‍

New research directions in pulmonary fibrosis

Several lines of investigation are converging on one idea: scarring is not a passive build up of tissue but an actively driven process, with switches that might be turned off to prevent damage.

YAP and TAZ: The molecular switches that could help halt lung scarring

YAP and TAZ are molecular switches inside cells that translate physical cues into instructions about growth and tissue building [15]. In 2015 they were identified as being some of the key regulators of fibroblast activation in pulmonary fibrosis.

Both proteins are found at high levels in scarred lung tissue, but not in healthy lung tissue - making them a potential candidate target for novel drug [16,17].

Preclinical work has also flagged other candidate compounds that dial this activity down, including trigonelline which is found in coffee (another win for the coffee drinkers) [18].

Vitronectin: Identifying culprit proteins in the scarring pathway

Australian research has added another piece. A Science Advances study co led by Associate Professor Liu at the University of Technology Sydney identified a lung protein called vitronectin that appears to switch on the scarring process [19] and is elevated in human IPF [20]. Identifying an upstream trigger is essential in treating such complex diseases, it offers a vital point of intervention before scarring, largely irreversible at this point in time, sets in [20].

What emerging research might mean for people living with pulmonary fibrosis

Most of these advanced approaches are at preclinical or early clinical trial stages, and their long term safety and effectiveness in humans has not yet been established.

Nevertheless, the level of understanding of the disease has significantly improved in the field.

Pulmonary fibrosis is increasingly understood as an actively maintained process with identifiable molecular switches, several of which can be manipulated in the laboratory. That reframing is what makes reversal a legitimate research question rather than wishful thinking.

Fibrosis is no longer viewed as inevitable, one directional scarring, even if reversibility is still yet to be achieved.

‍

‍

Disclaimer: The content provided on Diag-Nose.io is intended solely for informational and educational purposes. It does not constitute, and should not be relied upon as, medical advice, diagnosis, or treatment. Every effort is made to ensure the information provided is accurate and up-to-date. Users should consult a licensed physician or qualified healthcare provider before making any health-related decisions.

‍

References

  1. Pilarski, J. Q., Leiter, J. C., & Fregosi, R. F. (2019). Muscles of Breathing: Development, Function, and Patterns of Activation. Comprehensive physiology, 9(3), 1025–1080. https://doi.org/10.1002/cphy.c180008
  2. Lu, S., Liu, Y., Li, X., & Yao, Q. (2026). Treatment of pulmonary fibrosis: From disease mechanisms to future novel therapies (Review). International Journal of Molecular Medicine, 57(5), 112. https://doi.org/10.3892/ijmm.2026.5783
  3. Althobiani, M. A., Russell, A. M., Jacob, J., Ranjan, Y., Folarin, A. A., Hurst, J. R., & Porter, J. C. (2024). Interstitial lung disease: a review of classification, etiology, epidemiology, clinical diagnosis, pharmacological and non-pharmacological treatment. Frontiers in medicine, 11, 1296890. https://doi.org/10.3389/fmed.2024.1296890
  4. White E. S. (2015). Lung extracellular matrix and fibroblast function. Annals of the American Thoracic Society, 12 Suppl 1(Suppl 1), S30–S33. https://doi.org/10.1513/AnnalsATS.201406-240MG
  5. Moss, B. J., & Rosas, I. O. (2023). Defining the Genetic Landscape of Idiopathic Pulmonary Fibrosis: Role of Common and Rare Variants. American journal of respiratory and critical care medicine, 207(9), 1118–1120. https://doi.org/10.1164/rccm.202301-0177ED
  6. Palega SB, Borengasser AY and Sanders YY (2026) Senescent fibroblasts in aging and pulmonary fibrosis. Front. Aging 7:1816071. doi: 10.3389/fragi.2026.1816071
  7. Thannickal V. J. (2013). Mechanistic links between aging and lung fibrosis. Biogerontology, 14(6), 609–615. https://doi.org/10.1007/s10522-013-9451-6
  8. Venosa A. (2020). Senescence in Pulmonary Fibrosis: Between Aging and Exposure. Frontiers in medicine, 7, 606462. https://doi.org/10.3389/fmed.2020.606462
  9. Ajoolabady, A., Pratico, D., Bahijri, S. et al. Hallmarks and mechanisms of cellular senescence in aging and disease. Cell Death Discov. 11, 364 (2025). https://doi.org/10.1038/s41420-025-02655-x
  10. Nambiar A, Kellogg D III, Justice J, Goros M, Gelfond J, Pascual R, Hashmi S, Masternak M, Prata L, LeBrasseur N, et al: Senolytics dasatinib and quercetin in idiopathic pulmonary fibrosis: results of a phase I, single-blind, single-center, randomized, placebo-controlled pilot trial on feasibility and tolerability. Ebiomedicine. 90:1044812023
  11. Takeda, Y., Tsujino, K., Kijima, T., & Kumanogoh, A. (2014). Efficacy and safety of pirfenidone for idiopathic pulmonary fibrosis. Patient preference and adherence, 8, 361–370. https://doi.org/10.2147/PPA.S37233
  12. Wind, S., Schmid, U., Freiwald, M., Marzin, K., Lotz, R., Ebner, T., Stopfer, P., & Dallinger, C. (2019). Clinical Pharmacokinetics and Pharmacodynamics of Nintedanib. Clinical pharmacokinetics, 58(9), 1131–1147. https://doi.org/10.1007/s40262-019-00766-0
  13. Takehara, K., Koga, Y., Hachisu, Y., Utsugi, M., Sawada, Y., Saito, Y., Yoshimi, S., Yatomi, M., Shin, Y., Wakamatsu, I., Umetsu, K., Kouno, S., Nakagawa, J., Sunaga, N., Maeno, T., & Hisada, T. (2022). Differential Discontinuation Profiles between Pirfenidone and Nintedanib in Patients with Idiopathic Pulmonary Fibrosis. Cells, 11(1), 143. https://doi.org/10.3390/cells11010143
  14. Hoyer, N., Prior, T. S., Bendstrup, E., Wilcke, T., & Shaker, S. B. (2019). Risk factors for diagnostic delay in idiopathic pulmonary fibrosis. Respiratory research, 20(1), 103. https://doi.org/10.1186/s12931-019-1076-0
  15. Wu, C., Chen, X., Zhou, J., Wang, H., Huang, X., Tang, X., Cao, Z., & Ding, B.-S. (2026). Endothelial Hippo pathway regulates the neutrophil niche and lung fibrosis. Pharmacological Research, 227, 108169. https://doi.org/10.1016/j.phrs.2026.108169
  16. Papavassiliou, K. A., Sofianidi, A. A., Spiliopoulos, F. G., Gogou, V. A., Gargalionis, A. N., & Papavassiliou, A. G. (2024). YAP/TAZ Signaling in the Pathobiology of Pulmonary Fibrosis. Cells, 13(18), 1519. https://doi.org/10.3390/cells13181519
  17. Wagner, D.E., Alsafadi, H.N., Mitash, N. et al. Inhibition of epithelial cell YAP-TEAD/LOX signaling attenuates pulmonary fibrosis in preclinical models. Nat Commun 16, 7099 (2025). https://doi.org/10.1038/s41467-025-61795-x
  18. Zhang, F., Yue, H., Dong, R., He, J., Zhou, L., Dou, X., Wang, L., Zheng, P., Mao, Z., Zhu, X., Wang, Y., Liu, H., & Zhang, H. (2024). Trigonelline hydrochloride attenuates silica-induced pulmonary fibrosis by orchestrating fibroblast to myofibroblast differentiation. Respiratory research, 25(1), 242. https://doi.org/10.1186/s12931-024-02876-1
  19. University of Technology Sydney. (2026). New research clears the way to healing lung diseases. https://www.uts.edu.au/news/2026/07/new-research-clears-the-way-to-healing-lung-diseases
  20. Sean W. Cutter et al. ,Vitronectin metabolically programs profibrotic macrophages in 3D cultures and idiopathic pulmonary fibrosis.*Sci. Adv.*12,eaec8501(2026).DOI:10.1126/sciadv.aec8501

‍

About Diag-Nose.io

Diag-Nose.io, founded in 2020, is a TechBio company focused on translating the complexities of the unified airway into precision diagnostic and drug discovery solutions.

Their precision medicine technology combines advanced proteomics, computational biology, and AI (machine learning) to create a scalable respiratory biology model. This innovation aims to help clinicians prescribe the right treatments faster and enable researchers to accelerate the development of new therapies.

The company’s flagship platform, RhinoMAP™, leverages proteomic data to predict respiratory disease activity, monitor therapy response and predict treatment efficacy in advance, with an initial focus on anti-Th2 biologics.

Learn more at Diag-Nose.io

About the author

Beth Wright

Junior Researcher

Beth Wright, a Junior Researcher at Diag-Nose, expertly aims to improve accessibility of medical information and research in the field of Respiratory Disease.

Beth is completing a BBiomedSc. from Monash University.

‍

September 29, 2026  |  Read time: 6 mins

Beth Wright

‍

Healthy lungs are soft and elastic.

With the help of your diaphragm and various muscle groups they are pulled open when you breathe in and spring back when you breathe out [1].

What happens when lung elasticity is gone?

Pulmonary fibrosis is a debilitating disease that takes that soft elasticity away, replacing it with inflexible scar tissue (fibrosis). This scar tissue builds up between the lungs' air sacs, making lungs stiffer and harder to expand. As a result, breathing takes more effort and less oxygen can cross from the lungs into the bloodstream [2].

Pulmonary fibrosis is the most common, and serious, form of end stage interstitial lung disease (ILD).

Unpacking Interstitial Lung Disease (ILD) and its relation to pulmonary fibrosis

ILD is not just one disorder. ILD is the umbrella term for conditions that damage the tissue supporting the lungs' air sacs [3].

For the curious readers, you would be right to wonder what exactly the interstitium is.

In medical terms the lung interstitium is the space between the tiny air sacs in your lungs (the alveoli) and the small blood vessels surrounding them. The interstitium is essential as the oxygen from your alveoli passes through it into your blood, and in the same breath carbon dioxide moves into your air sacs.

Alveoli cannot regrow and once they are damaged, they are gone for good. This alone goes to show just how dangerous diseases of this nature can be. Some ILDs include:

What happens inside a lung with fibrosis?

Fibrosis begins when the delicate cells lining the air sacs are repeatedly injured. Where in a healthy lung, injury triggers a tidy repair process. In fibrosis, repair does not go so smoothly.

The repeated injury damages the lining cells of the alveoli, and faulty repair recruits fibroblasts, the cells that lay down structural tissue. Those fibroblasts pump out extracellular matrix [4], a mesh of proteins including collagen that normally holds tissue in shape. Too much of it fills spaces that should stay open and flexible.

The lung is rebuilt incorrectly, and gas exchange becomes progressively less efficient.

‍

Outside the lung, the lack of oxygen causes havoc on the body, leading to symptoms like weight loss, cyanosis (blue-tinted skin), fatigue, and even clubbed fingers [5].

‍

Why does pulmonary fibrosis develop?

There is no single cause, which is part of why it is hard to treat.

Current thinking is that fibrosis develops when someone genetically susceptible is exposed to damaging environmental factors over a long period [5].

Hence, several layers interact: inherited genetic variants, epigenetic changes (chemical markers that switch genes on and off without altering DNA itself), ageing, long term exposure to inhaled irritants, and immune dysfunction that keeps inflammation running [5].

Interestingly, ageing plays a particularly telling role in fibrosis development [6-8].

Fibroblasts taken from fibrotic lungs look prematurely old. They show markers of cellular senescence, a state in which a cell stops dividing but refuses to die [9]. These lingering cells release inflammatory signals that drive further scarring in the tissue around them. Drugs designed to clear them, called 'senolytics', are one experimental avenue under investigation [10].

Historically, the irreversible damage has meant a poor outlook for idiopathic pulmonary fibrosis (IPF) has been poor with median survival after diagnosis roughly three to five years. However, this number came about before the use of antifibrotics became more common. It’s important to note that averages cannot predict any individual's course, but it can help to explain the urgency in this field.

Are there treatment options improving prognoses?

‍

Pulmonary fibrosis treatment options available today

Antifibrotic drugs: pirfenidone and nintedanib

Two antifibrotic medications are currently approved, but they work quite differently [1, 10].

Pirfenidone slows fibroblasts from multiplying and reduces collagen production, largely by dampening TGF beta, one of the master switches for scarring [11]. Side effects include gastrointestinal upset and skin sensitivity.

Nintedanib blocks specific molecular signals that tell cells to grow and move, interrupting fibroblast growth, migration and the extracellular matrix production [12]. Its side effects, however, tend to be more pronounced than Pirfenidone [11], particularly diarrhoea, nausea and vomiting.

Both slow the decline in lung function, which is genuinely valuable. Neither relieves symptoms, and neither reverses existing scarring.

Yet, reported discontinuation rates sit between 10 and 20%, meaning a meaningful proportion of people stop taking the medication designed to help them [13]. That gap between what a drug does on a lung function chart and what a person feels day to day is the strongest argument for better options.

Supportive treatments for pulmonary fibrosis

Care may also include supplemental oxygen therapy to reduce breathlessness, pulmonary rehabilitation (a structured program of exercise training, breathing techniques and education), and lung transplantation in advanced disease.

Oxygen therapy delivers additional oxygen to your bloodstream when the lung scarring makes it hard for your body to get enough on its own.

Earlier detection matters in pulmonary fibrosis

Every strategy described here works better the earlier it is applied. Preventing scar tissue from forming is a far more tractable problem than dismantling it once set.

Yet, pulmonary fibrosis is frequently caught late [14]. Early symptoms, including breathlessness on exertion and a persistent dry cough, are easily attributed to ageing or a lingering infection. By the time imaging shows characteristic changes, meaningful lung tissue has often already been lost.

Closing that gap is one of the most valuable things respiratory medicine can do.

‍

New research directions in pulmonary fibrosis

Several lines of investigation are converging on one idea: scarring is not a passive build up of tissue but an actively driven process, with switches that might be turned off to prevent damage.

YAP and TAZ: The molecular switches that could help halt lung scarring

YAP and TAZ are molecular switches inside cells that translate physical cues into instructions about growth and tissue building [15]. In 2015 they were identified as being some of the key regulators of fibroblast activation in pulmonary fibrosis.

Both proteins are found at high levels in scarred lung tissue, but not in healthy lung tissue - making them a potential candidate target for novel drug [16,17].

Preclinical work has also flagged other candidate compounds that dial this activity down, including trigonelline which is found in coffee (another win for the coffee drinkers) [18].

Vitronectin: Identifying culprit proteins in the scarring pathway

Australian research has added another piece. A Science Advances study co led by Associate Professor Liu at the University of Technology Sydney identified a lung protein called vitronectin that appears to switch on the scarring process [19] and is elevated in human IPF [20]. Identifying an upstream trigger is essential in treating such complex diseases, it offers a vital point of intervention before scarring, largely irreversible at this point in time, sets in [20].

What emerging research might mean for people living with pulmonary fibrosis

Most of these advanced approaches are at preclinical or early clinical trial stages, and their long term safety and effectiveness in humans has not yet been established.

Nevertheless, the level of understanding of the disease has significantly improved in the field.

Pulmonary fibrosis is increasingly understood as an actively maintained process with identifiable molecular switches, several of which can be manipulated in the laboratory. That reframing is what makes reversal a legitimate research question rather than wishful thinking.

Fibrosis is no longer viewed as inevitable, one directional scarring, even if reversibility is still yet to be achieved.

‍

‍

Disclaimer: The content provided on Diag-Nose.io is intended solely for informational and educational purposes. It does not constitute, and should not be relied upon as, medical advice, diagnosis, or treatment. Every effort is made to ensure the information provided is accurate and up-to-date. Users should consult a licensed physician or qualified healthcare provider before making any health-related decisions.

‍

References

  1. Pilarski, J. Q., Leiter, J. C., & Fregosi, R. F. (2019). Muscles of Breathing: Development, Function, and Patterns of Activation. Comprehensive physiology, 9(3), 1025–1080. https://doi.org/10.1002/cphy.c180008
  2. Lu, S., Liu, Y., Li, X., & Yao, Q. (2026). Treatment of pulmonary fibrosis: From disease mechanisms to future novel therapies (Review). International Journal of Molecular Medicine, 57(5), 112. https://doi.org/10.3892/ijmm.2026.5783
  3. Althobiani, M. A., Russell, A. M., Jacob, J., Ranjan, Y., Folarin, A. A., Hurst, J. R., & Porter, J. C. (2024). Interstitial lung disease: a review of classification, etiology, epidemiology, clinical diagnosis, pharmacological and non-pharmacological treatment. Frontiers in medicine, 11, 1296890. https://doi.org/10.3389/fmed.2024.1296890
  4. White E. S. (2015). Lung extracellular matrix and fibroblast function. Annals of the American Thoracic Society, 12 Suppl 1(Suppl 1), S30–S33. https://doi.org/10.1513/AnnalsATS.201406-240MG
  5. Moss, B. J., & Rosas, I. O. (2023). Defining the Genetic Landscape of Idiopathic Pulmonary Fibrosis: Role of Common and Rare Variants. American journal of respiratory and critical care medicine, 207(9), 1118–1120. https://doi.org/10.1164/rccm.202301-0177ED
  6. Palega SB, Borengasser AY and Sanders YY (2026) Senescent fibroblasts in aging and pulmonary fibrosis. Front. Aging 7:1816071. doi: 10.3389/fragi.2026.1816071
  7. Thannickal V. J. (2013). Mechanistic links between aging and lung fibrosis. Biogerontology, 14(6), 609–615. https://doi.org/10.1007/s10522-013-9451-6
  8. Venosa A. (2020). Senescence in Pulmonary Fibrosis: Between Aging and Exposure. Frontiers in medicine, 7, 606462. https://doi.org/10.3389/fmed.2020.606462
  9. Ajoolabady, A., Pratico, D., Bahijri, S. et al. Hallmarks and mechanisms of cellular senescence in aging and disease. Cell Death Discov. 11, 364 (2025). https://doi.org/10.1038/s41420-025-02655-x
  10. Nambiar A, Kellogg D III, Justice J, Goros M, Gelfond J, Pascual R, Hashmi S, Masternak M, Prata L, LeBrasseur N, et al: Senolytics dasatinib and quercetin in idiopathic pulmonary fibrosis: results of a phase I, single-blind, single-center, randomized, placebo-controlled pilot trial on feasibility and tolerability. Ebiomedicine. 90:1044812023
  11. Takeda, Y., Tsujino, K., Kijima, T., & Kumanogoh, A. (2014). Efficacy and safety of pirfenidone for idiopathic pulmonary fibrosis. Patient preference and adherence, 8, 361–370. https://doi.org/10.2147/PPA.S37233
  12. Wind, S., Schmid, U., Freiwald, M., Marzin, K., Lotz, R., Ebner, T., Stopfer, P., & Dallinger, C. (2019). Clinical Pharmacokinetics and Pharmacodynamics of Nintedanib. Clinical pharmacokinetics, 58(9), 1131–1147. https://doi.org/10.1007/s40262-019-00766-0
  13. Takehara, K., Koga, Y., Hachisu, Y., Utsugi, M., Sawada, Y., Saito, Y., Yoshimi, S., Yatomi, M., Shin, Y., Wakamatsu, I., Umetsu, K., Kouno, S., Nakagawa, J., Sunaga, N., Maeno, T., & Hisada, T. (2022). Differential Discontinuation Profiles between Pirfenidone and Nintedanib in Patients with Idiopathic Pulmonary Fibrosis. Cells, 11(1), 143. https://doi.org/10.3390/cells11010143
  14. Hoyer, N., Prior, T. S., Bendstrup, E., Wilcke, T., & Shaker, S. B. (2019). Risk factors for diagnostic delay in idiopathic pulmonary fibrosis. Respiratory research, 20(1), 103. https://doi.org/10.1186/s12931-019-1076-0
  15. Wu, C., Chen, X., Zhou, J., Wang, H., Huang, X., Tang, X., Cao, Z., & Ding, B.-S. (2026). Endothelial Hippo pathway regulates the neutrophil niche and lung fibrosis. Pharmacological Research, 227, 108169. https://doi.org/10.1016/j.phrs.2026.108169
  16. Papavassiliou, K. A., Sofianidi, A. A., Spiliopoulos, F. G., Gogou, V. A., Gargalionis, A. N., & Papavassiliou, A. G. (2024). YAP/TAZ Signaling in the Pathobiology of Pulmonary Fibrosis. Cells, 13(18), 1519. https://doi.org/10.3390/cells13181519
  17. Wagner, D.E., Alsafadi, H.N., Mitash, N. et al. Inhibition of epithelial cell YAP-TEAD/LOX signaling attenuates pulmonary fibrosis in preclinical models. Nat Commun 16, 7099 (2025). https://doi.org/10.1038/s41467-025-61795-x
  18. Zhang, F., Yue, H., Dong, R., He, J., Zhou, L., Dou, X., Wang, L., Zheng, P., Mao, Z., Zhu, X., Wang, Y., Liu, H., & Zhang, H. (2024). Trigonelline hydrochloride attenuates silica-induced pulmonary fibrosis by orchestrating fibroblast to myofibroblast differentiation. Respiratory research, 25(1), 242. https://doi.org/10.1186/s12931-024-02876-1
  19. University of Technology Sydney. (2026). New research clears the way to healing lung diseases. https://www.uts.edu.au/news/2026/07/new-research-clears-the-way-to-healing-lung-diseases
  20. Sean W. Cutter et al. ,Vitronectin metabolically programs profibrotic macrophages in 3D cultures and idiopathic pulmonary fibrosis.*Sci. Adv.*12,eaec8501(2026).DOI:10.1126/sciadv.aec8501

‍

About Diag-Nose.io

Diag-Nose.io, founded in 2020, is a TechBio company focused on translating the complexities of the unified airway into precision diagnostic and drug discovery solutions.

Their precision medicine technology combines advanced proteomics, computational biology, and AI (machine learning) to create a scalable respiratory biology model. This innovation aims to help clinicians prescribe the right treatments faster and enable researchers to accelerate the development of new therapies.

The company’s flagship platform, RhinoMAP™, leverages proteomic data to predict respiratory disease activity, monitor therapy response and predict treatment efficacy in advance, with an initial focus on anti-Th2 biologics.

Learn more at Diag-Nose.io

About the author

Beth Wright

Junior Researcher

Beth Wright, a Junior Researcher at Diag-Nose, expertly aims to improve accessibility of medical information and research in the field of Respiratory Disease.

Beth is completing a BBiomedSc. from Monash University.

‍