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

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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

Original Articles

Burr hole drainage using urokinase for treatment of subacute subdural hematoma.: Min Su Kim, Seong Ho Kim, Oh Lyong Kim; Yeungnam Univ J Med. 2015;32(1):8-12. Published online June 30, 2015; DOI: https://doi.org/10.12701/yujm.2015.32.1.8

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Abstract PDF: BACKGROUND
Enlargement of subdural hematomas is relatively rapid in subacute stage of hematoma with clinical deterioration, which eventually necessitates surgery. The purpose of this study is to investigate the feasibility and safety of burr hole drainage using urokinase for management of patients with subacute subdural hematoma (SASDH). METHODS: Nine patients with SASDH were treated by burr hole drainage using urokinase. Under local anesthesia a catheter was inserted into the hematoma through a burr hole. Burr hole drainage was followed by hematoma thrombolysis with instillation of urokinase (10,000 units) every 12 hours. Drainage was discontinued when a significant decrease of hematoma was observed on cranial computed tomography. RESULTS: The patients' median age was 70 years (range, 62-87). The median Glasgow Coma Scale score before surgery was 15 (range, 11-15). Drainage was successfully performed in all patients. All patients had Glasgow Outcome Scale scores of 5 at discharge. There was no surgery-related morbidity or mortality. CONCLUSION: A burr hole drainage using urokinase could be a safe, feasible and effective minimally invasive method with low morbidity in treatment of selected patients with SASDHs.

Early or Late Gefitinib, Which is Better for Survival?: Retrospective Analysis of 228 Korean Patients with Advanced or Metastatic NSCLC.: Dong Gun Kim, Min Kyoung Kim, Sung Hwa Bae, Sung Ae Koh, Sung Woo Park, Hyun Je Kim, Myung Jin Kim, Hyo Jin Jang, Kyung Hee Lee, Kwan Ho Lee, Jin Hong Chung, Kyung Chul Shin, Hun Mo Ryoo, Myung Soo Hyun; Yeungnam Univ J Med. 2011;28(1):31-44. Published online June 30, 2011; DOI: https://doi.org/10.12701/yujm.2011.28.1.31

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Abstract PDF: BACKGROUND
The optimal timing of treatment with EGFR-tyrosine kinase inhibitors (EGFR-TKI) in NSCLC patients has not yet been determined. METHODS: We separated 228 patients with advanced/metastatic NSCLC treated with gefitinib into an early gefitinib group (patients who received gefitinib as first- or second-line treatment) and a delayed gefitinib group (patients who received gefitinib as third or fourth-line treatment) and attempted to determine whether the timing of gefitinib treatment affected clinical outcomes. RESULTS: Median overall survival (OS), progression free survival (PFS), and median OS from first-line treatment of advanced/metastatic disease (OSt) for 111 patients in the early gefitinib group were 6.2 months, 3.3 months, and 11.6 months. However, median OS, PFS, and OSt for 84 patients in the delayed gefitinib group were 7.8 months, 2.3 months, and 22.7 months. No differences in OS and PFS were observed between the 2 groups. However, OSt was significantly longer in the delayed gefitnib group. Timing of gefitinib therapy was one of the independent predictors of OSt. Hb > or = 10 g/dl, and having never smoked, and ECOG performance status < or =1 were independent predictors of better PFS. CONCLUSION: Deferral of gefitinib therapy in patients with advanced or metastatic NSCLC may be preferable if they are able to tolerate chemotherapy.

Differential Expression of Chemokines in Vascular Smooth Muscle Cells from Spontaneously Hypertensive Rat and Normotensive Rat: Jung Hae Kim, So Young Park, Hee Sun Kim; Yeungnam Univ J Med. 2007;24(2 Suppl):S373-383. Published online December 31, 2007; DOI: https://doi.org/10.12701/yujm.2007.24.2S.S373

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Abstract PDF: Background
：The action of chemokines to the vascular inflammation plays a pathogenic role in the development and maintenance of hypertension. Materials and methods：In the present study, the expression of chemokine IL-8/CXCL8, MCP-1/CCL2 and RANTES/CCL5 was investigated in cultured vascular smooth muscle cells (VSMC) obtained from the thoracic aorta of normotensive Wister-Kyoto rat (WKY) and spontaneously hypertensive rat (SHR). We used real-time PCR and western blotting.
Result
：The expressions of IL-8/CXCL8, and MCP-1/CCL2 mRNA were stronger in VSMC from SHR than in WKY. However, the expression of RANTES/CCL5 was stronger in VSMC from WKY than in SHR. Expressions of CXCR1, CCR2, CD14 and PPARγ mRNA were stronger in VSMC from WKY than in SHR. Expressions of LPS-induced IL-8/CXCL8 and MCP-1/CCL2 mRNA were stronger in VSMC from SHR, but expression of LPS-induced RANTES/CCL5 was stronger in VSMC from WKY. A PPAR-γ ligand, 15-deoxy-Δ12, 14- prostaglandin J2 (15d-PGJ2) which possesses anti-inflammatory activity suppressed the expressions of LPS-induced IL-8/CXCL8, MCP-1/CCL2 and RANTES/CCL5 in VSMC from WKY and the expressions of LPS-induced MCP-1/CCL2 and RANTES/CCL5 expressions in SHR. But, the expression of LPS-induced IL-8/CXCL8 mRNA in SHR was increased by 15d- PGJ2. Angiotensin II (AngII) also induced IL-8/CXCL8 and MCP-1/CCL2 mRNA expressions in VSMC from SHR, but inhibited the expression of RANTES/CCL5 mRNA. Activities of LPS, or AngII-induced MAP kinases were stronger in VSMC from SHR than in WKY. Expression of AngII-induced IL-8/CXCL8 mRNA was associated with ERK phathway, and the expression of AngII-induced MCP-1/CCL2 mRNA was associated with p38 pathway, and the inhibition of RANTES/CCL5 mRNA by AngII was not associated with MAP Kinases pathways.
Conclusion
：Chemokine IL-8/CXCL8 and MCP-1/CCL2, not RANTES/CCL5, has a possibility to play a critical role in the pathogenesis of hypertension in the SHR.

Diagnostic Efficiency of Lactate Dehydrogenase, Crreatine Kinase and Troponin T in Acute Myocardial Infarction.: Chae Hoon Lee, Kyung Dong Kim, Chung Sook Kim; Yeungnam Univ J Med. 1995;12(1):48-55. Published online June 30, 1995; DOI: https://doi.org/10.12701/yujm.1995.12.1.48

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Abstract PDF: The present study was designed to evaluate the efficiency of total lactate dehydrogenase, total creatine kinase, LD1/LD2 ratio, CK-MB and newly developed troponin T in acute myocardial infarction. The level of troponin T was 0.010.02 pg/L in 34 healthy person, but the peak vaule of acute myocardial infarction ranged in 4.7-24.2 pg/L. Total lactate dehydrogenase was peaked in 1 to 3 days after chest pain and then progressively decreased, but LD1/LD2 ratio was persistently higher than 1.0 for 10 days in most patients. Total creatine kinase and CK-MB were peaked in 1-2 days, and normalized in 3-4 days, so they, were useful in early diagnosis of acute myocardial infarction, but not for the late stages of acute myocardiz l infarction. Troponin T is early elevated and persistently high level for more than 10 days. Comparing with total lactate dehydrogenase, total creatine kinase, LD1/LD2 ratio and CK-MB, troponin-T test improves the efficiency of serodiagnostic method for the detection of ischemic myocardial damage.

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