Senescence in kidney ageing, injury and fibrosis: an abstract review
This abstract reviews evidence that chronic senescent cells are linked to kidney dysfunction and fibrosis in ageing and chronic kidney disease, while acute senescence supports repair; senescent-cell depletion in preclinical studies is described as a potential target. [1]
Automatic summary · not editorially reviewed
The key findings
Kidney ageing and CKD share capillary and epithelial cell loss, more fibroblasts, interstitial fibrosis and chronic immune infiltrates. [1]
Chronic senescent cells in human kidney ageing and CKD have been implicated as drivers of kidney dysfunction and fibrosis. [1]
Preclinical senescent-cell depletion studies show extended healthy lifespan, preserved function and reduced fibrosis in multiple organs, including the kidney. [1]
The source at a glance
- Study type / format
- Abstract of a narrative review
- Population / context
- People with kidney ageing and chronic kidney disease, plus preclinical models
- Summary based on
- Study abstract
- Original publication
- September 23, 2026
Shared features of kidney ageing and CKD
The abstract states that chronic kidney disease (CKD) remains incurable and progressive and affects about 850 million people worldwide. Kidney ageing and CKD share features such as loss of capillary and epithelial cells, more fibroblasts, interstitial fibrosis and chronic immune infiltrates. Finding pathways that drive fibrosis and loss of homeostasis in both states is described as a major research priority.
Supporting source [1]
Acute versus chronic senescence in the kidney
Cellular senescence is described as a generally irreversible growth arrest with an altered secretory phenotype, conserved across multicellular organisms. Acute senescence with prompt clearance is important for development, contributes to adaptive repair after organ injury and defends against neoplasia. In contrast, the increased senescent epithelial cells in human kidney ageing and CKD are said to include chronic senescent cells, which have been implicated as drivers of kidney dysfunction and fibrosis. Experimental evidence links chronic senescence to kidney leukocyte recruitment and myofibroblast activation.
Supporting source [1]
Preclinical depletion evidence and review scope
The abstract reports that preclinical studies depleting senescent cells show extended healthy lifespan, preserved function and reduced fibrosis in multiple organs, including the kidney. The authors say they examine current evidence of senescence as a driver of kidney disease and its potential as a therapeutic target. These depletion results come from preclinical studies and are not presented as proven human lifespan or treatment benefits.
Supporting source [1]
How to interpret this
This is an abstract only; the full text was not reviewed. Design, sample sizes, follow-up and outcome measures are not reported. The depletion findings are preclinical, and associations between senescence and kidney disease are not established causes.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Janas PP, Mason T, Ferenbach DA. · europepmc.org · September 23, 2026