NAMPT–SIRT2–lactate axis in senescence of human nucleus pulposus cells (abstract)
In this abstract, lactate treatment made cultured human nucleus pulposus cells senescent and activated p38-MAPK; NAMPT manipulation changed lactate and senescence in a SIRT2-dependent manner in vitro. Clinical relevance is unvalidated. [1]
Automatic summary · not editorially reviewed
The key findings
The abstract describes degenerated disc tissue samples and nucleus pulposus cells cultured in vitro and treated with lactate. [1]
Lactate was detected in all four degenerated disc tissue samples, with variable levels among individuals. [1]
The authors propose a NAMPT/SIRT2/lactate/p38-MAPK axis and say clinical relevance needs validation in larger cohorts with normal controls. [1]
The source at a glance
- Study type / format
- Laboratory study (abstract)
- Population / context
- Human degenerated intervertebral disc tissue and cultured human nucleus pulposus cells.
- Summary based on
- Study abstract
- Original publication
- September 1, 2026
Degenerated disc tissue and cultured nucleus pulposus cells
The abstract describes clinical degenerated intervertebral disc tissues plus nucleus pulposus cells cultured in vitro and treated with lactate. Lactate was measured with the WST-8 method, NAMPT and SIRT2 by western blotting, and senescence by senescence-associated β-galactosidase staining. Small interfering RNA and overexpression plasmids regulated NAMPT, combined with SIRT2 activators or inhibitors.
Supporting source [1]
Lactate, NAMPT and SIRT2 findings in vitro
Lactate was detected in all four degenerated disc tissue samples, with variable levels; NAMPT and SIRT2 showed similar expression patterns, which the authors say need larger cohorts. In vitro, lactate raised global protein lactylation, activated p38-MAPK and induced senescence. NAMPT knockdown reduced lactate and NAD levels; a SIRT2 activator partly restored the lactate decrease but not NAD. NAMPT overexpression caused lactate accumulation and senescence, antagonized by a lactate inhibitor or a SIRT2 inhibitor.
Supporting source [1]
Proposed axis and unvalidated clinical relevance
The authors conclude that in vitro NAMPT appears to modulate lactate metabolism in a SIRT2-dependent manner, activating p38-MAPK and contributing to nucleus pulposus cell senescence. They propose a functional NAMPT/SIRT2/lactate/p38-MAPK axis that may play a role in disc degeneration and could be a therapeutic target. They state that clinical relevance needs validation in larger patient cohorts with appropriate normal controls, and that in vivo validation and mechanistic details are still required.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Only four degenerated tissue samples are reported, without normal controls described here. The axis is proposed from in vitro experiments; in vivo validation and mechanistic details are stated as still required.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Zhang W, Mo L, Guo H, Zhang X, Tang H, Li W, Liu C. · europepmc.org · September 1, 2026