FGFR2

1 paper4 findings

HGNC 3689 NCBI Gene 2263 Taxon 9606

C, W, M, H: cells, worms or flies, mice, humans. Dark: independent labs found the same change there. Light: one lab or one study. Outline: nothing yet.

Labs are independent when their papers share no last author and no institution.

Against: findings that point the other way from most findings on the same outcome.

On aging: the drug’s trials ARN judged to be about aging, of every trial that tests it for any use.

No results posted: trials that ended more than a year ago with no results on ClinicalTrials.gov and no paper in ARN’s record.

Company ties: findings with an author at a company, or from a paper whose competing-interests statement declares ties to one.

A gene’s or a process’s line counts the gene with the processes named after it, as NLRP3 with the NLRP3 inflammasome, and the trials of drugs aimed at it.

1 lab in 1 country
3 trials

3 of 3 trials sponsored by developers of drugs on it

Animals1

Effects

3

Senescence-associated secretory phenotype (SASP)

upin cells1

1 study

FGFR2 induces senescence-associated secretory phenotype (SASP) in cells.
“Mechanistically, the alternative splicing-mediated switch from FGFR2-IIIb to FGFR2-IIIc established an FGF2-FGFR2-IIIc autocrine feedback loop, which drove ECs toward a senescence-associated secretory phenotype via the PKC (protein kinase C) ε/STAT3 (signal transducer and activator of transcription) pathway.”
Cellsvia PKCε/STAT3 pathway
RNA Splicing of the FGFR2 Gene Promotes Endothelial Cell Senescence and Atherosclerosis Development
Arteriosclerosis, thrombosis, and vascular biology19 Mar 2026

More on Senescence-associated secretory phenotype (SASP)

Cellular senescence

upin mice1

1 study

FGFR2 increases cellular senescence in mice.
“Notably, EC-specific knockout of FGFR2-IIIc in ApoE-/- mice reduced plaque area, suppressed senescence-associated secretory phenotype gene expression, and attenuated cellular senescence compared with controls.”
Animalsin ApoE-/- mice, shown by EC-specific knockout of FGFR2-IIIcvascular endothelium
RNA Splicing of the FGFR2 Gene Promotes Endothelial Cell Senescence and Atherosclerosis Development
Arteriosclerosis, thrombosis, and vascular biology19 Mar 2026

More on Cellular senescence

Atherosclerotic plaque area

upin mice1

1 study

FGFR2 increases atherosclerotic plaque area in mice.
“Notably, EC-specific knockout of FGFR2-IIIc in ApoE-/- mice reduced plaque area, suppressed senescence-associated secretory phenotype gene expression, and attenuated cellular senescence compared with controls.”
Animalsin ApoE-/- mice, shown by EC-specific knockout of FGFR2-IIIcvascular endothelium
RNA Splicing of the FGFR2 Gene Promotes Endothelial Cell Senescence and Atherosclerosis Development
Arteriosclerosis, thrombosis, and vascular biology19 Mar 2026

Associations

1

EC senescence

upin humans1

1 study

FGFR2 is associated with EC senescence.
“Elevated expression of the FGFR2-IIIc isoform was detected in clinical samples and animal models of aging and atherosclerosis, where it correlated with both EC senescence and atherosclerotic plaque formation.”
Humansin clinical samples and animal models of aging and atherosclerosis
RNA Splicing of the FGFR2 Gene Promotes Endothelial Cell Senescence and Atherosclerosis Development
Arteriosclerosis, thrombosis, and vascular biology19 Mar 2026

Latest

1 in 12 months

Arteriosclerosis, Thrombosis, and Vascular Biology19 Mar

RNA Splicing of the FGFR2 Gene Promotes Endothelial Cell Senescence and Atherosclerosis Development

Experiments in miceRNA splicing