The manipulation of ER stress-induced cell death as a therapeutic strategy for NSAIDs-induced intestinal ulcer.

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K19354
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Gastroenterology
• Research Institution: Osaka Medical College
• Principal Investigator: Yuichi Kojima 大阪医科大学, 医学部, 助教 (10747744)
• Research Collaborator: Nakagawa Takatoshi ; Harada Satoshi ; Asahi Michio ; Higuchi Kazuhide
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: ERストレス / オートファジー / NSAIDｓ誘引性小腸潰瘍

Outline of Final Research Achievements

Our aim was to discover a novel therapeutic molecular target for NSAIDs-induced intestinal ulcer. To achieve this, we explored how ER stress response, autophagy, and apoptosis were mutually interacted in the onset and development of the disorder. During a period of this grant, our colleagues reported that NSAIDs-induced intestinal ulcer was mitigated in intestine-specific autophagy-deficient mice, and a collagen loss caused by the fascinated turnover contributed to the onset of the disorder. Subsequently, we revealed that the fascinated turnover of collagen was caused by an E3 ligase, pVHL, which was published in peer-reviewed journal. Consequently, we could our research in review article in 2017. In addition, we published several clinical reports in regard to maximizing the established pharmacological therapy by using a state of art endoscopic investigation.

Free Research Field

下部消化管疾患