Journal of Yeungnam Medical Science

Focused 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.

Case Report

Rapidly resolved IgG4-related retroperitoneal fibrosis after steroid pulse therapy.: Soomin Jeung, Hyosang Kim, Yuri Seo, Hee Young Yoon, Nah Kyum Lee, Shinhee Park, Bomi Seo, Su Yeon Park, Su Kil Park; Yeungnam Univ J Med. 2016;33(1):40-43. Published online June 30, 2016; DOI: https://doi.org/10.12701/yujm.2016.33.1.40

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Abstract PDF: Retroperitoneal fibrosis (RF) is a disorder characterized by the presence of a retroperitoneal mass and concurrent systemic inflammation. Some cases of RF are recognized as belonging to the spectrum of immunoglobulin G4-related disease (IgG4-RD). Glucocorticoids are highly effective for treatment of retroperitoneal fibrosis, although the optimal dose and duration of therapy have not been established. An initial dose of prednisone (40-60 mg) daily is usually administered with a tapering scheme. We report on a 55-year-old man diagnosed with IgG4-related RF and successfully treated with a 3-day course of daily 250 mg (4 mg/kg) intravenous methylprednisolone, which resulted in the prompt resolution of urinary obstruction and systemic symptoms.

Original Article

Ultrastructural changes of fat-storing cells in experimental hepatic fibrosis.: Mi Jin Kim, Won Hee Choi, Tae Sook Lee; Yeungnam Univ J Med. 1992;9(2):224-238. Published online December 31, 1992; DOI: https://doi.org/10.12701/yujm.1992.9.2.224

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Abstract PDF: Hepatic fibrosis was induced in Sprague-Dawley rate to evaluate the ultrastructural changes of fat-storing cells (Ito cells). For experimental induction of liver fibrosis, the rats were administered intraperitoneally with 0.5 ml of 50% Ccl4 solution per Kg body weight, twice weekly for 12 weeks. The rats were sacrificed every week. The liver tissues were examined under light and electron microscopes. And the immunohistochemical study of desmin was also performed. The results were summarized as follows: Light microscopic findings: The cellular infiltrations was inflammatory cells and Kupffer cells developed from 1 week after Ccl4 injection, and were the most severe in 4 weeks. The strong immunoreactivity for desmin was also evident in 4 weeks. The centrilobular necrosis and fibrosis developed from 2 weeks after injection, and the necrosis persisted until 8 weeks. The progress of fibrosis was accompanied by decreases in cellular infiltration and reactivity for desmin, and increased gradual nodular formation was also observed. The cirrhosis was developed after 10 weeks. Electron microscopic findings: An increase in number of fat-storing cells was observed from 1 week after injection. Transitional cells characterized by a depletion of lipid droplets and a hypertrophy of the rER appeared after 2 weeks. The number of transitional cells with abundant collagen fibers in the extracellular spaces increased in 4 weeks. With progression of fibrosis the number of fat-strong cells decreased and proliferating fibroblasts with dilated rER were observed. According to these results it was revealed that there was an apparent transition from fatstrong cells to transitional cells and to fibroblasts. These cells had a few similar characteristics and may belong to the same cell population. Thus it was suggested that fatstrong cells might play an important role in hepatic fibrosis.

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