IJCEMR

Article http://dx.doi.org/10.26855/ijcemr.2024.04.006

Research Progress on Pathogenesis of Idiopathic Pulmonary Fibrosis Complicated with Lung Cancer

TOTAL VIEWS: 974

Shoushuo Fu, Chunlong Lin*, Qilong Ge, Huang Li, Keqin Hu, Chen Wang

Department of Respiratory and Critical Care Medicine, Yueyang Hospital Affiliated to Hunan Normal University, Yueyang, Hunan, China.

*Corresponding author: Chunlong Lin

Published: May 22,2024

Abstract

Idiopathic Pulmonary Fibrosis (IPF) is a fatal disease characterized by abnormal pulmonary fibroblast proliferation and excessive muscle fibroblast deposition in the extracellular matrix. Although it is not a malignant tumor, the prognosis is similar to many tumors or even worse. Sixty to seventy percent of IPF patients die from the disease. Without treatment, the average life expectancy after diagnosis is about 3-5 years. Other causes of death may be related to complications, with cardiovascular disease and Lung Cancer (LC) being the most significant contributors to mortality. At present, the pathogenesis of IPF-LC is not clear. Several studies have indicated the existence of a common pathway in the pathogenesis of IPF combined with LC. This review aims to provide a reference for the etiological treatment of IPF by examining relevant literature on the common pathogenesis and molecular pathways of IPF-LC, focusing on epigenetics, cellular communication, signaling pathways, and environmental factors.

References

[1] Caminati A, Lonati C, Cassandro R, et al. Comorbidities in idiopathic pulmonary fibrosis: an underestimated issue [J]. European Respiratory Review: An Official Journal of the European Respiratory Society, 2019, 28(153). 

[2] Zeltz C, Primac I, Erusappan P, et al. Cancer-associated fibroblasts in desmoplastic tumors: Emerging role of integrins [J]. Semin Cancer Biol., 2020, 62: 166-81.

[3] Velagacherla V, Mehta C H, Nayak Y, et al. Molecular pathways and role of epigenetics in the idiopathic pulmonary fibrosis [J]. Life Sci., 2022, 291: 120283.

[4] Vancheri C, Failla M, Crimi N, et al. Idiopathic pulmonary fibrosis: a disease with similarities and links to cancer biology [J]. The European Respiratory Journal, 2010, 35(3): 496-504.

[5] Kinoshita T, Goto T. Molecular Mechanisms of Pulmonary Fibrogenesis and Its Progression to Lung Cancer: A Review [J]. International Journal of Molecular Sciences, 2019, 20(6). 

[6] Otandault A, Anker P, Al Amir Dache Z, et al. Recent advances in circulating nucleic acids in oncology [J]. Ann Oncol., 2019, 30(3): 374-84.

[7] Totland M Z, Rasmussen N L, Knudsen L M, et al. Regulation of gap junction intercellular communication by connexin ubiquitination: physiological and pathophysiological implications [J]. Cellular and Molecular Life Sciences: CMLS, 2020, 77(4): 573-91.

[8] Chen Q, Boire A, Jin X, et al. Carcinoma-astrocyte gap junctions promote brain metastasis by cGAMP transfer [J]. Nature, 2016, 533(7604): 493-8.

[9] Hu L, Ding M, He W. Emerging Therapeutic Strategies for Attenuating Tubular EMT and Kidney Fibrosis by Targeting Wnt/beta-Catenin Signaling [J]. Frontiers in Pharmacology, 2021, 12: 830340.

[10] Shaikh T B, Kuncha M, Andugulapati S B, et al. Dehydrozingerone alleviates pulmonary fibrosis via inhibition of inflammation and epithelial-mesenchymal transition by regulating the Wnt/beta-catenin pathway [J]. Eur J Pharmacol., 2023, 953: 175820.

[11] Ballester B, Milara J, Cortijo J. Idiopathic Pulmonary Fibrosis and Lung Cancer: Mechanisms and Molecular Targets [J]. International Journal of Molecular Sciences, 2019, 20(3). 

[12] Chanda D, Otoupalova E, Smith S R, et al. Developmental pathways in the pathogenesis of lung fibrosis [J]. Molecular Aspects of Medicine, 2019, 65: 56-69.

[13] Wei K, Nguyen H N, Brenner M B. Fibroblast pathology in inflammatory diseases [J]. J Clin Invest., 2021, 131(20) 

[14] Chen P Y, Wei W F, Wu H Z, et al. Cancer-Associated Fibroblast Heterogeneity: A Factor That Cannot Be Ignored in Immune Microenvironment Remodeling [J]. Frontiers in Immunology, 2021, 12: 671595.

[15] Chen X, Song E. Turning foes to friends: targeting cancer-associated fibroblasts [J]. Nat Rev Drug Discov., 2019, 18(2): 99-115.

[16] Mahalanobish S, Saha S, Dutta S, et al. Matrix metalloproteinase: An upcoming therapeutic approach for idiopathic pulmonary fibrosis [J]. Pharmacol Res., 2020, 152: 104591.

[17] Li H X, Zheng J H, Fan H X, et al. Expression of alphavbeta6 integrin and collagen fibre in oral squamous cell carcinoma: association with clinical outcomes and prognostic implications [J]. J Oral Pathol Med., 2013, 42(7): 547-56.

[18] Ying H, Fang M, Hang Q Q, et al. Pirfenidone modulates macrophage polarization and ameliorates radiation-induced lung fibrosis by inhibiting the TGF-beta1/Smad3 pathway [J]. J Cell Mol Med., 2021, 25(18): 8662-75.

[19] Kinoshita T, Kudo-Saito C, Muramatsu R, et al. Determination of poor prognostic immune features of tumour microenvironment in non-smoking patients with lung adenocarcinoma [J]. European Journal of Cancer (Oxford, England: 1990), 2017, 86: 15-27.

[20] Hegde S, Leader A M, Merad M. MDSC: Markers, development, states, and unaddressed complexity [J]. Immunity, 2021, 54(5): 875-84.

[21] Fernandez I E, Greiffo F R, Frankenberger M, et al. Peripheral blood myeloid-derived suppressor cells reflect disease status in idiopathic pulmonary fibrosis [J]. The European Respiratory Journal, 2016, 48(4): 1171-83.

How to cite this paper

Research Progress on Pathogenesis of Idiopathic Pulmonary Fibrosis Complicated with Lung Cancer

How to cite this paper: Shoushuo Fu, Chunlong Lin, Qilong Ge, Huang Li, Keqin Hu, Chen Wang. (2024) Research Progress on Pathogenesis of Idiopathic Pulmonary Fibrosis Complicated with Lung CancerInternational Journal of Clinical and Experimental Medicine Research8(2), 227-231.

DOI: http://dx.doi.org/10.26855/ijcemr.2024.04.006