|Budget Amount *help
¥41,600,000 (Direct Cost: ¥32,000,000、Indirect Cost: ¥9,600,000)
Fiscal Year 2020: ¥8,060,000 (Direct Cost: ¥6,200,000、Indirect Cost: ¥1,860,000)
Fiscal Year 2019: ¥9,620,000 (Direct Cost: ¥7,400,000、Indirect Cost: ¥2,220,000)
Fiscal Year 2018: ¥9,620,000 (Direct Cost: ¥7,400,000、Indirect Cost: ¥2,220,000)
Fiscal Year 2017: ¥14,300,000 (Direct Cost: ¥11,000,000、Indirect Cost: ¥3,300,000)
|Outline of Final Research Achievements
Lesion of the heart after myocardial infarction is compensated by collagen. However, excess deposition of collagen is called as fibrosis that is a target of the treatment. Collagen is produced by myofibroblasts. Myocardial infarction results in death of cells at ischemic area, which causes inflammation. Inflammation is induced in parallel to progression of fibrosis that is controlled by myofibroblasts. Then, mechanistic analysis of inflammation is thought to be important to treat fibrosis. In addition to inflammation, concentration of proton is known to increase under the ischemic conditions. However, the physiological meaning has not been analyzed. In this project, importance of infiltration of leukocytes to ischemic area, the roles of proton-sensing receptor in myocardial infarction and receptor-mediated intracellular signaling were studied. Then, the association of these responses with fibrosis was evaluated.