NAT10 deficiency in aging drives impaired liver regeneration by disrupting PARP10 in an ac4C-dependent manner.

Qiang You, Cuicui Xiao, Haoqi Chen, Gongming Zhang, Feng Zhang, Zhengqi Wu, Yasong Liu, Jiebin Zhang, Haitian Chen, Jiaqi Xiao, Wenjie Chen, Jia Yao, Yingcai Zhang, Hua Li, Hui Li, Yang Yang, Rong Li, Jun Zheng

Department of Hepatic Surgery and Liver Transplantation Center of the Third Affiliated Hospital of Sun Yat-sen University; Organ Transplantation Research Center of Guangdong Province, Guangdong Province Engineering Laboratory for Transplantation Medicine. Guangzhou 510630, China.Department of Hepatic Surgery and Liver Transplantation Center of the Third Affiliated Hospital of Sun Yat-sen University; Organ Transplantation Research Center of Guangdong Province, Guangdong Province Engineering Laboratory for Transplantation Medicine. Guangzhou 510630, China. · pubmed

Paper

Abstract

The age-related decline in liver regenerative capacity worsens outcomes for elderly patients with liver disease or undergoing liver surgery, and therapeutic options are limited. The RNA modification N4-acetylcytidine (ac4C), catalyzed by N-acetyltransferase 10 (Nat10), is implicated in regeneration; however, its role in the aged liver remains unknown.

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Research summary

NAT10 deficiency impairs liver regeneration in aged mice by disrupting PARP10 function via ac4C modification. This study identifies a specific molecular mechanism underlying age-related decline in organ function, contributing to the understanding of how RNA modifications influence tissue homeostasis during aging.

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