What this means
This review suggests old, stuck cells may help connect kidney disease and heart stiffening. It does not prove that cause, and most cause-and-effect evidence comes from cells and animals.
Plain-English summary written by an AI model from the abstract. The original is below.
- Who it was tested in
- A review of earlier studies; mostly cell and animal work, plus some human samples
- Kind of research
- A study
The science
- Original title
- Cellular Senescence as a Core Mechanistic Link between CKD, Cardiac Fibrosis, and Aging.
- Authors
- Di Carmine S, Baird DP, Mylonas KJ
- Journal
- Kidney360
- Published
- Oct 23, 2026
- Study type
- Study
- PMID
- 42911667 ↗
Abstract
CKD and cardiovascular disease frequently coexist and represent a major global health burden. Cellular senescence may connect these disorders through persistent inflammation, fibrosis, and metabolic stress. Senescent cells undergo sustained proliferative arrest and release a pro-inflammatory, pro-fibrotic secretome called the senescence-associated secretory phenotype. In kidney and heart tissue, persistent senescent cells may promote immune-cell infiltration, fibroblast activation, extracellular matrix deposition, and tissue stiffening. Human biopsy, cardiac-tissue, urinary-biomarker, circulating-proteomic, and early senolytic data support associations between senescence markers, kidney dysfunction, and cardiovascular remodelling. However, most causal and interventional evidence still comes from cell-culture and animal models. This review critically evaluates cellular senescence as a plausible cardiorenal-fibrosis mechanism while emphasizing that causality, biomarker specificity, and therapeutic benefit in humans remain to be fully elucidated.
Di Carmine S, Baird DP, Mylonas KJ Cellular Senescence as a Core Mechanistic Link between CKD, Cardiac Fibrosis, and Aging. Kidney360. 2026. doi:10.34067/KID.0000001463. PMID: 42911667. https://pubmed.ncbi.nlm.nih.gov/42911667/
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