Review: NNMT as a stress-responsive regulator of tubular senescence in chronic kidney disease
This review summarizes largely correlative evidence that NNMT expression changes under stress and may link nicotinamide and methyl-donor metabolism to tubular senescence and fibrosis in chronic kidney disease. [1]
Automatic summary · not editorially reviewed
The key findings
The review describes senescence of renal tubular epithelial cells as a process linking chronic injury to fibrotic remodeling in chronic kidney disease. [1]
Reviewed studies suggest NNMT expression changes under stress, but the direction varies with cell type and context. [1]
The authors call current evidence largely correlative and suggest NNMT as a potential therapeutic target in chronic kidney disease. [1]
The source at a glance
- Study type / format
- Narrative review (abstract)
- Population / context
- Renal tubular epithelial cells and people with chronic kidney disease, as discussed in the review
- Summary based on
- Study abstract
- Original publication
- June 22, 2026
NNMT in stressed kidney tubule cells
The review addresses chronic kidney disease, which the authors describe as persistent cellular stress, tubular dysfunction and progressive tubulointerstitial fibrosis. They present senescence of renal tubular epithelial cells as a process linking chronic injury to fibrotic remodeling. NNMT, an enzyme that methylates nicotinamide, has drawn attention for a possible role in stress-associated metabolic and epigenetic regulation. The authors summarize current evidence on stress-responsive NNMT regulation and discuss its possible involvement in tubular senescence during disease progression.
Supporting source [1]
Variable NNMT direction; NAD and methyl donor effects
According to the reviewed studies, NNMT expression can change dynamically under various stress conditions, but the direction of change varies with cell type and context. Through consumption of nicotinamide and S-adenosylmethionine, sustained NNMT activation may influence nicotinamide adenine dinucleotide (NAD) homeostasis, methyl donor balance and homocysteine metabolism. The authors suggest this could in turn affect redox regulation, epigenetic remodeling and senescence-associated signaling pathways. They also discuss possible interactions between NNMT-associated metabolic dysregulation, chronic stress responses, tubular senescence and fibrosis.
Supporting source [1]
Correlative evidence and a potential target
The authors state that current evidence is largely correlative. On that basis they suggest NNMT may be a stress-associated metabolic regulator and a potential therapeutic target in chronic kidney disease. The abstract reports no human trial, no treatment results and no measured outcomes; it describes a review of existing evidence rather than new experiments.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. The evidence described is largely correlative, and the abstract reports no human trial, treatment results or measured outcomes.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Liu A, Zhu XJ, Sun WD, Bi SZ, Zhang CY, Li JH. · europepmc.org · June 22, 2026