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Therapeutic potential of targeting kinase inhibition in patients with idiopathic pulmonary fibrosis

Yeungnam University Journal of Medicine 2020년 37권 4호 p.269 ~ 276
김수지, 임재향, 우정훈,
소속 상세정보
김수지 ( Kim Su-Ji ) - Yeungnam University College of Medicine Department of Pharmacology
임재향 ( Lim Jae-Hyang ) - Ewha Womans University College of Medicine Department of Microbiology
우정훈 ( Woo Chang-Hoon ) - Yeungnam University College of Medicine Department of Pharmacology

Abstract


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-β) 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-β-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.

키워드

Fibrosis; Idiopathic pulmonary fibrosis; Kinase; Transforming growth factor beta

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