Mouse and cell study: NMN reduced LPS-induced liver injury via STING-ACSL4
In LPS-treated mice and cells, NMN reversed ferroptosis and inflammation and destabilized the STING-ACSL4 complex; this is preclinical evidence, not proof of benefit in human sepsis. [1]
Automatic summary · not editorially reviewed
The key findings
In mouse and cell models, LPS triggered ferroptosis and inflammation in macrophages and hepatocytes, and macrophage signals worsened hepatocyte ferroptosis. [1]
NMN suppressed mtDNA-mediated cGAS-STING activation and weakened the STING-ACSL4 interaction, which the authors link to reduced ferroptosis. [1]
The authors conclude that NMN protects against LPS-induced acute liver injury by suppressing cGAS-STING inflammation and weakening the STING-ACSL4 interaction. [1]
The source at a glance
- Study type / format
- Preclinical mouse and in vitro study (abstract)
- Population / context
- Mice with LPS-induced liver injury and cultured primary hepatocytes, primary macrophages and THP-1 cells.
- Summary based on
- Study abstract
- Original publication
- September 14, 2026
LPS liver injury in mice and cultured cells
The abstract describes mouse models of liver injury induced by LPS (lipopolysaccharide) plus in vitro models using primary hepatocytes, primary macrophages and THP-1 cells. LPS triggered ferroptosis and inflammation in both macrophages and hepatocytes, and paracrine inflammatory signals from macrophages further worsened hepatocyte ferroptosis. NMN (nicotinamide mononucleotide) effectively reversed these pathological changes. The abstract does not report sample sizes, doses or follow-up.
Supporting source [1]
NMN weakened STING-ACSL4 and cGAS-STING signaling
Mechanistically, NMN suppressed mtDNA-mediated activation of cGAS-STING and weakened the interaction between STING and ACSL4. Several laboratory methods together indicated that NMN destabilized the STING-ACSL4 complex, thereby restraining ferroptosis. The authors conclude that NMN protects against LPS-induced acute liver injury by suppressing cGAS-STING-mediated inflammation and weakening the pro-ferroptotic STING-ACSL4 interaction. These are proposed mechanisms from cell and mouse experiments, not established human treatments.
Supporting source [1]
Abstract-only preclinical scope of the NMN findings
The source is an abstract; the full text was not reviewed. It reports mouse and cell experiments on LPS-induced acute liver injury, so the findings concern this preclinical model and do not show that NMN prevents or treats liver damage or sepsis in people. The abstract gives no human data, no clinical outcomes and no information on safety or dosing.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Findings come from mouse models and cultured cells, with no reported sample sizes, doses, follow-up or human data. Mechanisms are proposed, not established treatments.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Liao Y, Zhu CL, Zhang WZ, Cheng LD, Liu Y, Wang Y, Zhou T, Zhao JX, Bian JJ, Zou Z, Zhou M. · europepmc.org · September 14, 2026