AUF1 Restrains Hepatocyte Senescence by Maintaining Mitochondrial Homeostasis in AML12 Hepatocyte Model.

Myeongwoo Jung, Sukyoung Han, Seungyeon Ryu, Seongho Cha, Ye Eun Sim, Se Hoon Jung, Hyosun Tak, Wook Kim, Eun Kyung Lee

Department of Biochemistry, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.Department of Biochemistry, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea. · pubmed

Paper

Abstract

Cellular senescence, a hallmark of aging, involves irreversible growth arrest and an enhanced senescence-associated secretory phenotype (SASP). It is often accompanied by mitochondrial dysfunction and altered inter-organelle communication. Using a chronic oxidative stress model in AML12 hepatocytes, we confirmed senescence by canonical assays (e.g., SA β-gal positivity and proliferation arrest) and observed a decline in the RNA-binding protein AUF1 (hnRNP D). AUF1 knockdown further amplified senescent phenotypes, including elongation of mitochondrial network, loss of mitochondrial membrane potential, reduced ATP level, and elevated mitochondrial reactive oxygen species (ROS). In addition, AUF1 knockdown weakened mitochondria-endoplasmic reticulum coupling and reduced mitochondrial Ca

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Research summary

The paper claims that AUF1 plays a crucial role in restraining hepatocyte senescence by maintaining mitochondrial homeostasis. This research is relevant as it addresses the mechanisms underlying cellular senescence, a key aspect of aging, and explores potential interventions that could mitigate age-related cellular dysfunction.

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