이영선 교수

Abstract Since its discovery in 2012, ferroptosis has been well characterized by the accumulation of lipid peroxides due to the failure of glutathione-dependent antioxidant defenses. It is known as an iron-dependent form of programmed cell death, which is distinct from other forms of cell death such as apoptosis and necrosis. Nonetheless, little is known about the ferroptotic agent-induced endoplasmic reticulum (ER) stress response and its role in cell death. Recent studies reveal that the ferro

Non-alcoholic fatty liver disease (NAFLD) is a dominant cause of chronic liver disease, but the exact mechanism of progression from simple steatosis to nonalcoholic steatohepatitis (NASH) remains unknown. Here, we investigated the role of exosomes in NAFLD progression. Exosomes were isolated from a human hepatoma cell line treated with palmitic acid (PA) and their miRNA profiles examined by microarray. The human hepatic stellate cell (HSC) line (LX-2) was then treated with exosome isolated from

Quiescent hepatic stellate cells (HSCs) in healthy liver store 80% of total liver retinols and release them depending on the extracellular retinol status. However, HSCs activated by liver injury lose their retinols and produce a considerable amount of extracellular matrix, subsequently leading to liver fibrosis. Emerging evidence suggests that retinols and their metabolites such as retinoic acids (RAs) contribute to liver regeneration, fibrosis and tumor. However, it is not clear yet why HSCs lo

Liver fibrosis is a common result of liver injury owing to various kinds of chronic liver diseases. A deeper understanding of the pathophysiology of liver fibrosis and identifying potential therapeutic targets of liver fibrosis is important because liver fibrosis may progress to advanced liver diseases, such as cirrhosis and hepatocellular carcinoma. Despite numerous studies, the underlying mechanisms of liver fibrosis remain unclear. Mechanisms of the development and progression of liver fibros

Ferroptosis is considered genetically and biochemically distinct from other forms of cell death. In this study, we examined whether ferroptosis shares cell death pathways with other types of cell death. When human colon cancer HCT116, CX-1, and LS174T cells were treated with ferroptotic agents such as sorafenib (SRF), erastin, and artesunate, data from immunoblot assay showed that ferroptotic agents induced endoplasmic reticulum (ER) stress and the ER stress response-mediated expression of death

Abstract The expression of chemokine receptor CX 3 CR1 is related to migration and signaling in cells of the monocyte-macrophage lineage. The precise roles of CX 3 CR1 in the liver have been investigated but not clearly elucidated. Here, we investigated the roles of CX 3 CR1 in hepatic macrophages and liver injury. Hepatic and splenic CX 3 CR1 low F4/80 low monocytes and CX 3 CR1 low CD16 − monocytes were differentiated into CX 3 CR1 high F4/80 high or CX 3 CR1 high CD16 + macrophages by co-cult

Anoctamin-1 (ANO1) acts as a Ca(2+)-activated Cl(-) channel in various normal tissues, and its expression is increased in several different types of cancer. Therefore, understanding the regulation of ANO1 surface expression is important for determining its physiological and pathophysiological functions. However, the trafficking mechanism of ANO1 remains elusive. Here, we report that segment a (N-terminal 116 amino acids) of ANO1 is crucial for its surface expression, and we identified 14-3-3γ as

Ferroptosis has been reported as a unique form of cell death. However, in recent years, researchers have increasingly challenged the uniqueness of ferroptosis compared to other types of cell death. In this study, we examined whether ferroptosis shares cell death pathways with other types of cell death, especially autophagy, via the autophagic process. Here, we observed that ferroptosis inducers (artesunate [ART] and erastin [ERA]) and autophagy inducers (bortezomib [BOR] and XIE62-1004) led to a

Dimethyl fumarate (DMF), which has been approved by the Food and Drug Administration for the treatment of relapsing-remitting multiple sclerosis, is considered to exert anti-inflammatory and antioxidant effects. Microglia maintain homeostasis in the central nervous system and play a key role in neuroinflammation, while autophagy controls numerous fundamental biological processes, including pathogen removal, cytokine production, and clearance of toxic aggregates. However, the role of DMF in autop

Breast cancer is the most common cancer among women worldwide, and it is a main cause of death in women. As with breast cancer, metabolic components are important risk factors for the development of nonalcoholic fatty liver disease (NAFLD). In this retrospective cohort study, we aimed to determine the prevalence of NAFLD in patients with breast cancer and the impact of NAFLD on the prognosis of breast cancer.Patients with breast cancer were enrolled in the study from January 2007 to June 2017. H

INTRODUCTION: Because nonalcoholic fatty liver disease (NAFLD) is becoming a leading cause of chronic liver disease, noninvasive evaluations of its severity are immediately needed. This prospective cross-sectional study evaluated the effectiveness of noninvasive assessments of hepatic steatosis, fibrosis, and steatohepatitis. METHODS: Patients underwent laboratory tests, liver biopsy, transient elastography, and MRI. Multiparametric MR was used to measure MRI proton density fat fraction, MR spec