Mouse study: endothelial C/EBPβ/AEP pathway linked to vascular aging and shorter lifespan
In mice, progressive activation of the C/EBPβ/AEP pathway in aging vascular endothelial cells was linked to vascular degeneration and reduced lifespan; blocking the pathway or supplementing NMN alleviated age-related vascular decline in this abstract. [1]
Automatic summary · not editorially reviewed
The key findings
The abstract reports progressive activation of the C/EBPβ/AEP pathway in aging vascular endothelial cells, linked to vascular degeneration and reduced lifespan. [1]
In mice, endothelial-specific overexpression of C/EBPβ or AEP accelerated vascular aging and shortened lifespan. [1]
In endothelial-specific Tie 2-C/EBPβ transgenic mice, AEP ablation or an AEP-resistant NAMPT mutant ameliorated vascular aging and extended lifespan; CP#11A or NMN alleviated age-related vascular decline, with CP#11A more effective. [1]
The source at a glance
- Study type / format
- Preclinical mouse study (abstract)
- Population / context
- Mice, including endothelial-specific Tie 2-C/EBPβ transgenic mice; aging vascular endothelial cells.
- Summary based on
- Study abstract
- Original publication
- September 16, 2026
Aging endothelial cells and the C/EBPβ/AEP pathway
The abstract describes age-related microvascular dysfunction that disrupts nutrient homeostasis and waste clearance and can lead to organ failure. It states that a critical gap remains in understanding which molecular drivers cause vascular deterioration and how they drive aging across the organism. The authors report progressive activation of the C/EBPβ/AEP pathway in aging vascular endothelial cells and link it to vascular degeneration and reduced lifespan.
Supporting source [1]
Mouse experiments: overexpression, NAMPT cleavage and NAD depletion
In mice, endothelial-specific overexpression of C/EBPβ or AEP accelerated vascular aging and shortened lifespan. Mechanistically, AEP is reported to cleave NAMPT, the rate-limiting enzyme in NAD biosynthesis, resulting in systemic NAD depletion and senescence that elicits central and peripheral vascular dysfunction and ultimately systemic aging. Genetic ablation of AEP or expression of an AEP-resistant NAMPT N136A mutant significantly ameliorated vascular aging and extended lifespan in endothelial-specific Tie 2-C/EBPβ transgenic mice.
Supporting source [1]
Pharmacological results in mice and abstract-only scope
Pharmacologically, the AEP inhibitor CP#11A or nicotinamide mononucleotide (NMN) supplementation alleviated age-related vascular decline in mice, with CP#11A showing superior efficacy. The authors propose a model in which endothelial senescence contributes to vascular dysfunction and systemic aging via C/EBPβ/AEP signaling, and name C/EBPβ/AEP as a therapeutic target. These are preclinical mouse findings reported in an abstract; the full text was not reviewed, and no human outcomes are described.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. All findings are preclinical mouse data; no human outcomes, sample sizes, follow-up or effect sizes are reported in the abstract. Associations and proposed mechanisms are not proof of cause in humans, and NMN or CP#11A are not established human treatments.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Li B, Nie S, Wang M, An J, Qian Z, Meng X, Edgington-Mitchell LE, Zhang Z, Yang X, Ye K. · europepmc.org · September 16, 2026