HINT1 suppression protects against age-related cardiac dysfunction by enhancing mitochondrial biogenesis.

Michio Sato, Tsuyoshi Kadomatsu, Jun Morinaga, Yuya Kinoshita, Daisuke Torigoe, Haruki Horiguchi, Sumio Ohtsuki, Shuji Yamamura, Ryoko Kusaba, Takanori Yamaguchi, Goro Yoshioka, Kimi Araki, Tomohiko Wakayama, Keishi Miyata, Koichi Node, Yuichi Oike

Department of Molecular Genetics, Kumamoto University, Kumamoto, Japan; Center for Metabolic Regulation of Healthy Aging (CMHA), Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan; Division of Kumamoto Mouse Clinic (KMC), Institute of Resource Developmental and Analysis (IRDA), Kumamoto University, Kumamoto, Japan; Department of Cardiovascular Medicine, School of Medicine, Saga University, Saga, Japan.Department of Molecular Genetics, Kumamoto University, Kumamoto, Japan; Center for Metabolic Regulation of Healthy Aging (CMHA), Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan; Division of Kumamoto Mouse Clinic (KMC), Institute of Resource Developmental and Analysis (IRDA), Kumamoto University, Kumamoto, Japan; Department of Cardiovascular Medicine, School of Medicine, Saga University, Saga, Japan. · pubmed

Paper

Abstract

Cardiac function declines with age, impairing exercise tolerance and negatively impacting healthy aging. However, mechanisms driving age-related declines in cardiac function are not fully understood.

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Research summary

HINT1 suppression enhances mitochondrial biogenesis to protect against age-related cardiac dysfunction. This research addresses a mechanism related to aging and cardiac health, contributing to the understanding of age-related decline in cardiac function.

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