β-Nicotinamide mononucleotide prevents senescence and lipid accumulation in hepatic stellate cells by restoring SIRT1 function.

Tomofumi Saka, Riri Hayashi, Yuta Yoshino, Taichi Mitsui, Hiroe Maruyama, Hiroyuki Kono, Mitsuyasu Kawaguchi, Hidehiko Nakagawa, Akira Ikari, Satoshi Endo

Laboratory of Biochemistry, Gifu Pharmaceutical University, Gifu, 501-1196, Gifu, Japan. · pubmed

Paper

Abstract

The activation of hepatic stellate cells (HSCs) plays a vital role in liver wound healing, including liver regeneration and repair. However, as senescent cells increase with the continued activation, the secretion of extracellular matrix, collagen, transforming growth factor-β, and other cytokines increases, leading to liver fibrosis, cirrhosis, and liver cancer. This study investigated the effects of lipid peroxidation-derived aldehydes (LPDAs) such as 4-hydroxy-2-nonenal (HNE) and 4-oxo-2-nonenal (ONE), which accumulate with aging, on HSC senescence. Additionally, it investigated the inhibitory effects of nicotinamide mononucleotide (NMN), a precursor of NAD

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper claims that β-Nicotinamide mononucleotide prevents senescence and lipid accumulation in hepatic stellate cells by restoring SIRT1 function. This research is relevant as it addresses the mechanisms of cellular senescence and potential interventions that could mitigate age-related liver dysfunction, contributing to the understanding of aging processes.

Author of this paper? Send a correction.