TABLE 1.

KLF5‐related animal models

Animal models	Organization types	Phenotypes	References
Klf5 knockout mice	Embryo	Mouse with homozygous knockout of Klf5 died before embryonic day 8.5.	12
	Blood vessel	The medial and adventitial layers of the aortic wall of Klf5 +/− mice are abnormally thinned and dilated; in response to vascular injury, the activation, proliferation, inflammation, and angiogenesis of fibroblasts and smooth muscle cells are impaired.	12
	Heart	Klf5 +/− mice have reduced heart weight, reduced fibrosis, and thinner heart ventricular walls.	12
	Gastrointestinal tract	Klf5 +/− mice have malformed gastrointestinal villi, and decrease the number of extracellular matrix and mesenchymal cells.	12
	Mammary gland	Klf5 mammary gland‐specific knockout mice can be observed to inhibit ductal elongation at 9 wk of age; the lobular alveolar structure is significantly reduced during pregnancy and lactation; the production of whey acidic protein (WAP) in mice during pregnancy and lactation is decrease, and there is a defect in milk secretion. Klf5 knockout decreased the proliferation, survival and stemness of mammary epithelial cells.	7
	Adipose tissue	The development of white adipose tissue in Klf5 +/− mice is delayed, and lipid droplets in adipocytes are reduced. Klf5 +/− mice can avoid obesity, hypercholesterolemia and impaired glucose tolerance caused by high fat.	13
	Skeleton	Klf5 deficiency impairs cartilage degradation and calcification in the perinatal period.	194
	Lung	The fetal lung airway epithelial cells in transgenic mice with specific knockout of Klf5 have inhibited lung maturation during the cystic development stage. Phenotypic abnormalities appear in different components of bronchiolar smooth muscle, pulmonary blood vessels, and respiratory epithelium. Mice with knocked out both alleles of Klf5 died of respiratory distress immediately after birth. Klf5 is essential for lung function and morphogenesis.	19
	Intestine	Intestinal‐specific deletion of Klf5 using Villin‐Cre showed that Klf5 is required to maintain gut epithelial cell proliferation, differentiation, and positioning along the crypt radial axis; Klf5 deletion in the intestinal epithelium using Shh‐Cre inhibited villus morphogenesis and epithelial differentiation; depletion of Klf5 disrupts the integrity of intestinal stem cells.	16, 17, 18
	Hematopoietic system	Knockout mice of Klf5 have enlarged spleens and increased peripheral white blood cells; the proportion of eosinophils is significantly increased, while the proportion of neutrophils is downregulated, long‐term hematopoietic progenitor cells are reduced, and the ability to reproduce is reduced.	195
	Eye	Klf5 was specifically deleted in the ectoderm‐derived structure of the ocular surface of mice, resulting in eyelid defects with malformed meibomian glands, corneal abnormalities, and loss of conjunctival goblet cells; Klf5 contributed to corneal epithelial homeostasis via regulating the expression of desmosomal components.	196, 197
	Prostate	Prostate‐specific Klf5 heterozygous deletion mice induced hyperplasia with thicker cell layers in the lateral prostate, anterior prostate, and dorsal prostate; Klf5 homozygous deletion caused prostate epithelial cell apoptosis instead of hyperplasia.	14
Klf5 transgenic (Tg) mice	Prostate	Knockin of the Klf5 K358R gene in mouse model, the prostate has changed, showing a lighter, smaller and denser tissue morphology; prostate cells were reduced, the acinar area was smaller, and increased differentiation of basal cells into luminal cells.	15
	Skin	Klf5 transgenic mice showed craniofacial defects, extracerebral malformations, persistent abdominal herniation, and ectodermal dysplasia; overexpression of Klf5 in adult mice resulted in hair follicle occlusion, hyperkeratosis and epidermal erosion.	198
	Esophagus	Esophageal epithelial cells specifically overexpress Klf5 in ED‐L2/Klf5 mouse suprabasal cells without proliferation, but have increased proliferation of basal cells.	199