最先端研究セミナー

招聘者： 伊藤 尚基 プロジェクトリーダー(国立長寿医療研究センター　ジェロサイエンス研究センター　中枢性老化-骨格筋代謝-運動機能制御研究プロジェクトチーム)

演題：Novel molecular pathogenesis of sarcopenia induced by impaired liver-skeletal muscle crosstalk during aging

日時：2026年2月25日（水）　12：00-13：00

開催場所：発生医学研究所1階　カンファレンス室

※ZOOMミーティングのURLはMoodleの「S-HIGO最先端研究セミナーA、B」にてご確認ください。

https://md.kumamoto-u.ac.jp/course/view.php?id=120331

Abstract：

Sarcopenia is a progressive disease characterized by an age-related decline in skeletal muscle function. The fundamental molecular pathogenesis of sarcopenia remains unclear. Our research focuses on the age-related impairment of nicotinamide adenine dinucleotide (NAD+) metabolism and inter-organ communication in sarcopenia during aging1,2. In this study, I will discuss about the novel molecular pathogenesis of sarcopenia, lactic acidosis in skeletal muscle, which is caused by impaired liver-skeletal muscle crosstalk. Systemic lactate tolerance was decreased in aged mice due to the impaired liver lactate processing capacity, which caused the accumulation of lactate and intracellular acidification, lactic acidosis, in skeletal muscle. This lactic acidosis in skeletal muscle leads to decreased NAD+ levels and subsequent skeletal muscle dysfunction. Crucially, the pharmacological activation of hypoxia-inducible factor (HIF) or the liver-specific activation of HIF1α improved age-related impairment in lactate tolerance, lactic acidosis in skeletal muscle, and sarcopenia. Our results demonstrate that lactic acidosis in skeletal muscle is a novel molecular cause of sarcopenia and highlight HIF1α in the liver as a pharmacological target for treating sarcopenia.

担当分野：筋発生再生　小野（6601)