Journal of Yeungnam Medical Science

Review article

Therapeutic potential of targeting kinase inhibition in patients with idiopathic pulmonary fibrosis: Suji Kim, Jae Hyang Lim, Chang-Hoon Woo; Yeungnam Univ J Med. 2020;37(4):269-276. Published online July 22, 2020; DOI: https://doi.org/10.12701/yujm.2020.00458

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Fibrosis is characterized by excessive accumulation of extracellular matrix components. The fibrotic process ultimately leads to organ dysfunction and failure in chronic inflammatory and metabolic diseases such as pulmonary fibrosis, advanced kidney disease, and liver cirrhosis. Idiopathic pulmonary fibrosis (IPF) is a common form of progressive and chronic interstitial lung disease of unknown etiology. Pathophysiologically, the parenchyma of the lung alveoli, interstitium, and capillary endothelium becomes scarred and stiff, which makes breathing difficult because the lungs have to work harder to transfer oxygen and carbon dioxide between the alveolar space and bloodstream. The transforming growth factor beta (TGF-) signaling pathway plays an important role in the pathogenesis of pulmonary fibrosis and scarring of the lung tissue. Recent clinical trials focused on the development of pharmacological agents that either directly or indirectly target kinases for the treatment of IPF. Therefore, to develop therapeutic targets for pulmonary fibrosis, it is essential to understand the key factors involved in the pathogenesis of pulmonary fibrosis and the underlying signaling pathway. The objective of this review is to discuss the role of kinase signaling cascades in the regulation of either TGF--dependent or other signaling pathways, including Rho-associated coiled-coil kinase, c-jun N-terminal kinase, extracellular signal-regulated kinase 5, and p90 ribosomal S6 kinase pathways, and potential therapeutic targets in IPF.

Citations

Citations to this article as recorded by

Targeting Growth Factor and Cytokine Pathways to Treat Idiopathic Pulmonary Fibrosis
Hongbo Ma, Shengming Liu, Shanrui Li, Yong Xia
Frontiers in Pharmacology.2022;[Epub] CrossRef
Vitamin D3 alleviates pulmonary fibrosis by regulating the MAPK pathway via targeting PSAT1 expression in vivo and in vitro
Wenxiang Zhu, Qi Ding, Lu Wang, Gonghao Xu, Yirui Diao, Sihao Qu, Sheng Chen, Yuanyuan Shi
International Immunopharmacology.2021; 101: 108212. CrossRef
Advances in the science and treatment of respiratory diseases
Jin Hong Chung
Yeungnam University Journal of Medicine.2020; 37(4): 251. CrossRef
Effects of Pirfenidone and Nintedanib on Markers of Systemic Oxidative Stress and Inflammation in Patients with Idiopathic Pulmonary Fibrosis: A Preliminary Report
Alessandro G. Fois, Elisabetta Sotgiu, Valentina Scano, Silvia Negri, Sabrina Mellino, Elisabetta Zinellu, Pietro Pirina, Gianfranco Pintus, Ciriaco Carru, Arduino A. Mangoni, Angelo Zinellu
Antioxidants.2020; 9(11): 1064. CrossRef

Review

Role of the transforming growth factor (TGF)-β1 and TGF-β1 signaling pathway on the pathophysiology of respiratory pneumococcal infections: Maria Jose Andrade, Jae Hyang Lim; Yeungnam Univ J Med. 2017;34(2):149-160. Published online December 31, 2017; DOI: https://doi.org/10.12701/yujm.2017.34.2.149

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Abstract PDF: Streptococcus pneumoniae, pneumococcus, is the most common cause of community-acquired pneumonia (CAP). CAP is an important infectious disease with high morbidity and mortality, and it is still one of the leading causes of death worldwide. Many genetic factors of the host and various environmental factors surrounding it have been studied as important determinants of the pathophysiology and outcomes of pneumococcal infections. Various cytokines, including transforming growth factor (TGF)-β1, are involved in different stages of the progression of pneumococcal infection. TGF-β1 is a cytokine that regulates a wide range of cellular and physiological functions, including immune and inflammatory responses. This cytokine has long been known as an anti-inflammatory cytokine that is critical to preventing the progression of an acute infection to a chronic condition. On the other hand, recent studies have unveiled the diverse roles of TGF-β1 on different stages of pneumococcal infections other than mitigating inflammation. This review summarizes the recent findings of the role of TGF-β1 on the pathophysiology of pneumococcal infections, which is fundamental to developing novel therapeutic strategies for such infections in immune-compromised patients.

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