|Budget Amount *help
¥17,290,000 (Direct Cost: ¥13,300,000、Indirect Cost: ¥3,990,000)
Fiscal Year 2020: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2019: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2018: ¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2017: ¥9,490,000 (Direct Cost: ¥7,300,000、Indirect Cost: ¥2,190,000)
|Outline of Final Research Achievements
Mitochondrial oxidative phosphorylation underlies sustained ATP production, which has been implicated in the pathogenesis of cardiovascular disease such as heart failure (HF) after myocardial infarction (Circulation 2018; Cell Commun Signal 2019; Eur J Pharmacol 2020; Front Cardiovasc Med 2020; Circ Heart Fail 2021; Commun Biol 2021; Cardiovasc Res 2021). Mitochondrial complex I have been intensively investigated for their roles in inducing impaired mitochondrial respiration in HF. In this study, we showed the latest data on the pathobiology of complex assembly in mediating mitochondrial dysfunction processes, focusing on the central role of mitochondrial complex II (Cell Commun Signal 2019; Biochem Biophys Rep 2020). An improved understanding of these mechanisms might facilitate the development of novel therapeutic agents or diets targeting mitochondrial complex assembly, which could be effective in the prevention and treatment of skeletal muscle abnormalities in HF.