Chelating intracellular calcium reduces fibroblast senescence and eases lung fibrosis
Treating cells and an in vivo fibrosis model with a calcium chelator delayed senescence markers, reduced collagen buildup, and dampened inflammatory secretions.
Biochimica et Biophysica Acta General Subjects
In experiments using cultured fibroblasts and an in vivo animal model, researchers examined how intracellular calcium changes during cellular senescence and pulmonary fibrosis. They measured free calcium levels during senescence and observed a significant increase. Chelating this intracellular calcium buildup delayed the elevation of calcium, lowered reactive oxygen species accumulation, decreased DNA damage, and slowed fibroblast senescence. In the animal model, intraperitoneal administration of the calcium chelator BAPTA-AM markedly alleviated pulmonary fibrosis. The treatment reduced body weight loss, inflammatory cell infiltration, and collagen deposition, while lowering senescence and fibrosis markers. Transcriptomic analysis of fibrotic lung tissues confirmed that BAPTA-AM treatment also significantly suppressed the senescence-associated secretory phenotype.
Why it matters
Intracellular calcium signaling is a known feature of cellular senescence, but its operational role in fibrotic lung pathology has been unclear. These findings show that directly curbing calcium accumulation can restrain senescence markers and lessen tissue remodeling in age-associated diseases.
Caveats
The findings are limited to cell culture and an animal model, meaning effects may differ in clinical human settings. The abstract also does not evaluate long-term safety, optimal dosing, or whether the treatment can reverse advanced fibrosis.
The paper
Yangzhou University
Biochimica et Biophysica Acta General Subjects · 30 Sep 2026
