Protein weakens growth-factor signaling in human artery cells
In experiments with human artery cells, blocking a protein released by cells that stopped dividing restored signaling from insulin-like growth factor 1.
Our read
Interventions- Studied:
- Experiments in cells
- Why it’s aging research:
- It studies something that builds up in the body with age.
Editor of record: Boris Djordjevic · AgingResearch.News
Human smooth muscle cells from the aorta, the body's main artery, received insulin-like growth factor 1, a growth-related protein, in laboratory experiments. Researchers induced senescence, a state in which cells stop dividing, with bleomycin. They tested the growth factor at 0, 10, 50 and 100 nanograms per milliliter. Higher doses reduced senescence more.
Senescent cells released more insulin-like growth factor binding protein 7, a protein that inhibits growth-factor signaling. Fluid collected from these cells weakened the signaling response. An antibody against the binding protein restored it. Separately, atherosclerotic pigs given the growth factor had more collagen-producing smooth muscle cells in plaque caps and fewer fat-filled immune cells in plaque cores, alongside lower activity of senescence-related genes.
Why it matters
Senescent cells contribute to a cycle of inflammation and plaque progression in atherosclerosis. The authors suggest that targeting the binding protein could restore growth-factor sensitivity and help interrupt that cycle.
Caveats
The antibody experiments tested signaling in lab-grown cells, not whether blocking the protein reduced senescence or stabilized plaques. The plaque findings came from pigs, not people, and the work was reported in a conference abstract.
The paper
Tulane Univ; Tulane Univ Sch of Medicine
AHA Scientific Sessions 2026 Abstract, Nov 2, 2026
Presented at AHA Scientific Sessions 2026, abstract 15848
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