Table. 2 Disease phenotypes resulting from TFF3 deficiency.

Gastrointestinal research

Oral dextran sulfate sodium

Colitis

Poor epithelial regeneration leading to widespread death from colitis.

[15]

Radiation and chemotherapy

Intestinal mucositis

It is very sensitive to chemotherapy- and radiotherapy-induced mucositis.

[16]

Oral dextran sulfate sodium

Colitis

Leads to complete suppression of TLR2-mediated anti-apoptosis in acute mucosal inflammation

[67]

Colonic apoptosis increased, but expression of receptor-related or stress-related cell death regulators did not change significantly.

[131]

Oral Toxoplasma gondii

Ileitis

IFN-γ, IL-12, IL-1β, and TNF-α gene expression decreased, and ileal CD4⁺ lymphocyte count reduced.

[132]

It induced decrease in TFF1 and TFF2 levels in the stomach. Trefoil peptides may individually regulate transcription of the entire family.

[133]

Metabolism research

Body weight was significantly lower than that of wild-type mice. Metabolic-pathway-related genes were significantly dysregulated.

[18]

Accumulation of fatty acids in the liver was affected, and metabolism-related gene expression was reduced.

[33]

Injection of tunicamycin

Acute endoplasmic reticulum stress

Decreased ability for pro-inflammatory cascade initiation.

[34]

Nervous system research

High-salt diet combined with transient occlusion of middle cerebral artery

Stroke

TFF3 depletion impaired vascular function and worsened stroke outcomes.

[20]

Ischemia/reperfusion

Brain Injury

Cell death, cerebral infarction, and forelimb motor deficits were more severe.

[21]

Alkali and laser

Corneal Injury

Re-epithelialization of corneal wounds is significantly prolonged.

[17]

Exhibited accelerated presbycusis and more pronounced high-frequency hearing loss.

[39]

Loudspeaker

Hearing impaired

Presbycusis-related gene expression was significantly downregulated by TFF3 deletion.

[40]