Thymic Bmi-1 hampers γδT17 generation and its derived RORγt-IL-17A signaling to delay cardiac aging.

Qiuyi Wang, Yue Wang, Yujie Lin, Jiawen Zhou, Zhiyuan Mao, Xin Gu, Haiyun Chen, Jiyu Li, Ao Chen, Jin'ge Zhang, Rong Wang, Yingming Zhao, Mufeng Gu, Qing Li, Yongjie Zhang, Jianliang Jin

Department of Human Anatomy, School of Basic Medical Sciences, Key Laboratory for Aging and Disease, Nanjing Medical University, Nanjing, Jiangsu 211166, China.Department of Human Anatomy, School of Basic Medical Sciences, Key Laboratory for Aging and Disease, Nanjing Medical University, Nanjing, Jiangsu 211166, China. · pubmed

Paper

Abstract

New immunosenescence targets for preventing senescence-associated pathological cardiac hypertrophy (SA-PCH) need to be explored. In the present study, with physiologically aged human and mouse samples, the IL-17A level increased with physiological aging, heart failure (HF), and SA-PCH and was negatively correlated with thymic Bmi-1 expression.

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Research summary

Thymic Bmi-1 expression negatively regulates IL-17A levels, which are associated with cardiac aging and hypertrophy. The study explores mechanisms related to immunosenescence and their impact on age-related cardiac conditions, addressing potential root causes of aging.

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