Aging aggravates aortic aneurysm and dissection via miR-1204-MYLK signaling axis in mice

Ze-Long Liu, Yan Li, Yi-Jun Lin, Mao-Mao Shi, Meng-Xia Fu, Zhi-Qing Li, Da-Sheng Ning, Xiang-Ming Zeng, Xiang Liu, Qing-Hua Cui, Yue-Ming Peng, Xin-Min Zhou, Ye-Rong Hu, Jia-Sheng Liu, Yu-Jia Liu, Mian Wang, Chun-Xiang Zhang, Wei Kong (), Zhi-Jun Ou () and Jing-Song Ou ()
Additional contact information
Ze-Long Liu: Sun Yat-sen University
Yan Li: Sun Yat-sen University
Yi-Jun Lin: Sun Yat-sen University
Mao-Mao Shi: Sun Yat-sen University
Meng-Xia Fu: Sun Yat-sen University
Zhi-Qing Li: Peking University
Da-Sheng Ning: Sun Yat-sen University
Xiang-Ming Zeng: Sun Yat-sen University
Xiang Liu: Sun Yat-sen University
Qing-Hua Cui: Peking University
Yue-Ming Peng: Sun Yat-sen University
Xin-Min Zhou: The Second Xiangya Hospital of Central South University
Ye-Rong Hu: The Second Xiangya Hospital of Central South University
Jia-Sheng Liu: Sun Yat-sen University
Yu-Jia Liu: Sun Yat-sen University
Mian Wang: National-Guangdong Joint Engineering Laboratory for Diagnosis and Treatment of Vascular Diseases
Chun-Xiang Zhang: Rush University Medical Center
Wei Kong: Peking University
Zhi-Jun Ou: National-Guangdong Joint Engineering Laboratory for Diagnosis and Treatment of Vascular Diseases
Jing-Song Ou: Sun Yat-sen University

Nature Communications, 2024, vol. 15, issue 1, 1-21

Abstract: Abstract The mechanism by which aging induces aortic aneurysm and dissection (AAD) remains unclear. A total of 430 participants were recruited for the screening of differentially expressed plasma microRNAs (miRNAs). We found that miR-1204 is significantly increased in both the plasma and aorta of elder patients with AAD and is positively correlated with age. Cell senescence induces the expression of miR-1204 through p53 interaction with plasmacytoma variant translocation 1, and miR-1204 induces vascular smooth muscle cell (VSMC) senescence to form a positive feedback loop. Furthermore, miR-1204 aggravates angiotensin II-induced AAD formation, and inhibition of miR-1204 attenuates β-aminopropionitrile monofumarate-induced AAD development in mice. Mechanistically, miR-1204 directly targets myosin light chain kinase (MYLK), leading to the acquisition of a senescence-associated secretory phenotype (SASP) by VSMCs and loss of their contractile phenotype. MYLK overexpression reverses miR-1204-induced VSMC senescence, SASP and contractile phenotypic changes, and the decrease of transforming growth factor-β signaling pathway. Our findings suggest that aging aggravates AAD via the miR-1204-MYLK signaling axis.

Date: 2024
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DOI: 10.1038/s41467-024-50036-2

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