Calcium chelation in senescent fibroblasts and mouse lung fibrosis
In this abstract, senescent fibroblasts showed higher intracellular calcium; chelating calcium reduced senescence markers in cells and, given intraperitoneally to mice, alleviated fibrosis phenotypes. These are preclinical findings, not evidence of benefit in human aging. [1]
Automatic summary · not editorially reviewed
The key findings
Intracellular calcium levels measured during senescence showed a significant increase. [1]
Chelating senescence-induced calcium accumulation delayed calcium elevation and reduced ROS, DNA damage and fibroblast senescence. [1]
In mice, intraperitoneal BAPTA-AM alleviated pulmonary fibrosis phenotypes and suppressed the senescence-associated secretory phenotype. [1]
The source at a glance
- Study type / format
- Preclinical laboratory and mouse study (abstract)
- Population / context
- Senescent fibroblasts in cell experiments and mice with pulmonary fibrosis phenotypes
- Summary based on
- Study abstract
- Original publication
- September 30, 2026
Calcium rise measured in senescent fibroblasts
The abstract states that calcium regulators and downstream intracellular calcium signaling are a hallmark feature of cellular senescence, but changes in free intracellular calcium during senescence and age-related disease remain incompletely understood, especially in fibroblasts. The researchers measured intracellular calcium levels during senescence and observed a significant increase. This describes a measurement in cells, not an outcome in people.
Supporting source [1]
Chelation reduced senescence signs in cells and mouse fibrosis
Chelating the calcium accumulation caused by senescence stimuli delayed the calcium rise and also reduced reactive oxygen species accumulation, DNA damage and fibroblast senescence. In mice, intraperitoneal BAPTA-AM (BAPTA) markedly alleviated pulmonary fibrosis phenotypes: less body-weight loss, fewer infiltrating inflammatory cells, less collagen deposition and lower fibrosis and senescence marker expression. Lung tissue analysis also showed suppressed senescence-associated secretory phenotype (SASP). These are associations in a preclinical model, not proven causes or human benefits.
Supporting source [1]
Abstract-only scope of the calcium chelator findings
The authors conclude that restricting intracellular calcium accumulation after senescence triggers can mitigate fibroblast senescence and ameliorate pulmonary fibrosis, and highlight therapeutic potential of calcium chelators in age-associated pathologies. Only the abstract was reviewed; the full text was not reviewed. The abstract does not report human participants, dosing for people, or long-term outcomes, so the proposed therapeutic potential is not established.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Findings come from cell experiments and mice, with no human participants, human dosing or long-term outcomes reported. Associations do not establish causation or human benefit.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Xu J, Yang J, Sun W, Shi Q, Ni Q, Chen J, Luan C, Ma X, Yang C. · europepmc.org · September 30, 2026