The Claim
Pericytes in the choroid of patients with neovascular AMD and smoke-exposed mice exhibit increased expression of fibroblast and contractile markers (e.g., COL1A1, α-SMA), contributing to vascular instability and fibrosis in the disease process.
What the research says
Supports is higher
Support is ahead, but a single strong opposing study can change this.
These are independent scores, not a percentage. Higher-grade studies count more, so a single strong opposing study can outweigh several weaker ones.
In individuals with neovascular age-related macular degeneration and in mice exposed to smoke, choroidal pericytes show elevated levels of fibroblast and contractile proteins, which are associated with blood vessel instability and tissue scarring.
See the scientific wording
Pericytes in the choroid of patients with neovascular AMD and smoke-exposed mice exhibit a distinct activated phenotype characterized by increased expression of fibroblast and contractile markers (e.g., COL1A1, α-SMA), suggesting they contribute to vascular instability and fibrosis in the disease process.
Smoking causes immune cells to release a signal that binds to support cells around blood vessels in the eye, making those cells stiff and scar-like. These changed cells pull on blood vessels, cause them to leak, and lay down scar tissue, which leads to abnormal blood vessel growth and vision loss.
What the research says
1 studyIn people and mice with a serious eye disease called wet AMD, smoking causes special support cells around blood vessels in the eye to become stiff and scar-like, making the blood vessels leak more. The study shows this happens because of a specific chemical signal turned on by smoking.
Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting studies
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