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Review
. 2023 Apr 24;28(9):3674.
doi: 10.3390/molecules28093674.

Recent Advances (2015-2020) in Drug Discovery for Attenuation of Pulmonary Fibrosis and COPD

Affiliations
Review

Recent Advances (2015-2020) in Drug Discovery for Attenuation of Pulmonary Fibrosis and COPD

Atukuri Dorababu et al. Molecules. .

Abstract

A condition of scarring of lung tissue due to a wide range of causes (such as environmental pollution, cigarette smoking (CS), lung diseases, some medications, etc.) has been reported as pulmonary fibrosis (PF). This has become a serious problem all over the world due to the lack of efficient drugs for treatment or cure. To date, no drug has been designed that could inhibit fibrosis. However, few medications have been reported to reduce the rate of fibrosis. Meanwhile, ongoing research indicates pulmonary fibrosis can be treated in its initial stages when symptoms are mild. Here, an attempt is made to summarize the recent studies on the effects of various chemical drugs that attenuate PF and increase patients' quality of life. The review is classified based on the nature of the drug molecules, e.g., natural/biomolecule-based, synthetic-molecule-based PF inhibitors, etc. Here, the mechanisms through which the drug molecules attenuate PF are discussed. It is shown that inhibitory molecules can significantly decrease the TGF-β1, profibrotic factors, proteins responsible for inflammation, pro-fibrogenic cytokines, etc., thereby ameliorating the progress of PF. This review may be useful in designing better drugs that could reduce the fibrosis process drastically or even cure the disease to some extent.

Keywords: COPD; Smad signaling pathway; TGF-β1; collagen deposition; pulmonary fibrosis.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Illustration of the pathways of biomarkers that lead to PF/IPF (adapted from Zhou et al. [4]).

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References

    1. Hubbard R., Cooper M., Antoniak M., Venn A., Khan S., Johnston I., Lewis S., Britton J. Risk of cryptogenic fibrosing alveolitis in metal workers. Lancet. 2000;355:466–467. doi: 10.1016/S0140-6736(00)82017-6. - DOI - PubMed
    1. Goemaere N.N.T., Grijm K., van Hal P.T.W., den Bakker M.A. Nitrofurantoin-induced pulmonary fibrosis: A case report. J. Med. Case Rep. 2008;2:169. doi: 10.1186/1752-1947-2-169. - DOI - PMC - PubMed
    1. Jin Y.-K., Li X.-H., Wang W., Liu J., Zhang W., Fang Y.-S., Zhang Z.-F., Dai H.-P., Ning W., Wang C. Follistatin-Like 1 Promotes Bleomycin-Induced Pulmonary Fibrosis through the Transforming Growth Factor Beta 1/Mitogen-Activated Protein Kinase Signaling Pathway. Chin. Med. J. 2018;131:1917–1925. doi: 10.4103/0366-6999.238151. - DOI - PMC - PubMed
    1. Zhou Z., Kandhare A.D., Kandhare A.A., Bodhankar S.L. Hesperidin ameliorates bleomycin-induced experimental pulmonary fibrosis via inhibition of TGF-beta1/Smad3/AMPK and IkappaBalpha/NF-kappaB pathways. EXCLI J. 2019;18:723–745. doi: 10.17179/excli2019-1094. - DOI - PMC - PubMed
    1. Richeldi L., Costabel U., Selman M., Kim D.S., Hansell D.M., Nicholson A.G., Brown K.K., Flaherty K.R., Noble P.W., Raghu G., et al. Efficacy of a Tyrosine Kinase Inhibitor in Idiopathic Pulmonary Fibrosis. N. Engl. J. Med. 2011;365:1079–1087. doi: 10.1056/NEJMoa1103690. - DOI - PubMed