| 研究課題/領域番号 |
22K16408
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| 研究種目 |
若手研究
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| 配分区分 | 基金 |
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| 審査区分 |
小区分54040:代謝および内分泌学関連
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| 研究機関 | 富山大学 |
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研究代表者 |
NAWAZ ALLAH 富山大学, 学術研究部医学系, 助教 (80881482)
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| 研究期間 (年度) |
2022-04-01 – 2023-03-31
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| 研究課題ステータス |
中途終了 (2022年度)
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| 配分額 *注記 |
4,550千円 (直接経費: 3,500千円、間接経費: 1,050千円)
2024年度: 1,430千円 (直接経費: 1,100千円、間接経費: 330千円)
2023年度: 1,300千円 (直接経費: 1,000千円、間接経費: 300千円)
2022年度: 1,820千円 (直接経費: 1,400千円、間接経費: 420千円)
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| キーワード | Muscle Regenration / NAD metabolism / Muscle Stem Cell / Immune cells / Aging |
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| 研究開始時の研究の概要 |
Aging-related decline in NAD+ is reported to impair regenerative process. CD38 is an ectoenzyme to degrade NAD+ and is reportedly increased in inflammatory macrophages during aging. In this study, I will clarify the role of CD38 in the regulation of muscle stem cell functions in aged mice. Thus, my study may provide a clue that inhibition of CD38 restore functions of aged muscle stem cell functions. Reduction in CD38 boosts NAD+ and may rescue aging- and obesity-induced delay in muscle regeneration. Metabolic reprogramming in macrophages could open new field to boost the regenerative process.
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| 研究実績の概要 |
Previous reports show macrophages-derived signals are crucial for regeneration process. Both macrophages and satellite cells require nicotinamide adenine dinucleotide (NAD+) for their biological functions. Aging-related decline in NAD+ is reported to impair regenerative process and significantly inhibits satellite cells differentiation. Administration of NAD+ precursors restore NAD+ deficiency in aged muscle and also enhances recovery process. CD38 is an ectoenzyme to degrade NAD+ and is reportedly increased in inflammatory macrophages during aging. However, how inhibition of CD38 affects satellite cells functions in aging-induced delay in recovery process, remain elusive. We are currently investigating how deletion of CD38 in aged mice affect regenerative capacity of muscle stem cells. Our initial results reveal that blocking/inhibition of CD38 results in restoration of NAD+ and muscle stem cell functions.
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