Deletion of Nrf1α exacerbates oxidative stress-induced cellular senescence by disrupting cell homeostasis.

Da Lyu, Meng Wang, Lu Qiu, Rongzhen Deng, Shaofan Hu, Yiguo Zhang

The Laboratory of Cell Biochemistry and Topogenetic Regulation, College of Bioengineering, Chongqing University, No. 174 Shazheng Street, Shapingba District, Chongqing 400044, China. Electronic address: [email protected]. · pubmed

Paper

Abstract

Cellular senescence is recognized as a fundamental hallmark contributing to ageing and various age-related diseases, with oxidative stress playing a critical initiating role in their pathological processes. However, the anti-senescence potential of the antioxidant nuclear factor erythroid-derived 2-like 1 (Nrf1, encoded by Nfe2l1) remains elusive, despite accumulating evidence demonstrating its role as an indispensable redox-determining transcription factor for maintaining cellular homeostasis and organ integrity. This study reveals that deletion of Nrf1α significantly elevates senescence characteristics in Nrf1α

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Research summary

Deletion of Nrf1α exacerbates oxidative stress-induced cellular senescence by disrupting cell homeostasis. This paper is relevant as it investigates the role of a transcription factor in cellular senescence, which is a fundamental aspect of aging and age-related diseases, potentially addressing root causes of these processes.

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