TABLE 3.
Disease | Experimental model | Experimental aim | Conclusion | References |
---|---|---|---|---|
AMD | The mice of targeted deletion of macrophage Abca1 and Abcg1 | The effect of deletion of Abca1 and Abcg1 on cholesterol homeostasis. | The lack of Abca1 and Abcg1 will lead to cholesterol accumulation and trigger early AMD. | 163 |
The potential function of ABCA1 in the eye. | Impaired activity of the ABCA1‐mediated lipid efflux pathway may contribute to the progression of AMD. | 164 | ||
Human iPSC‐derived RPE cells of Abca1 deletion | The identification of conditions for reducing the expression and function of ABCA1 in RPE. | The deletion of Abca1 leads to intracellular lipid accumulation and promotes the development of AMD. | 165 | |
The mice of Tspo knockout | The impact of Tspo knockout on RPE in mice. | The lack of TSPO in mice leads to the defect of cholesterol efflux in RPE cells and induces the onset of AMD. | 166 | |
Cataract | Male and female Sprague–Dawley rats | The mechanism of cataract induced by E2012. | The reduction of cholesterol in lens has been proved to be a prerequisite for cataract induced by E2012. | 167 |
Male Sprague–Dawley rats | The relationship between lens opacity and cholesterol biosynthesis inhibition. | The inhibition of cholesterol biosynthesis is one of the reasons for lens turbidity. | 168 | |
The knock‐in mouse model with G589S mutation in Lss | The roles of LSS in cataractogenesis. | The down‐regulation of cholesterol biosynthesis may lead to the lens development defect during cataract. | 169 | |
The Shumiya cataract rat | The mechanism of cataract formation. | Cholesterol in the lens may be important for maintaining normal lens homeostasis. | 170 | |
Corneal diseases | To understand abnormal cholesterol accumulation in cornea. | LCAT, ApoD, ApoA1 and ABCA1 are essential to prevent cholesterol accumulation and maintain vision. | 171 | |
DES | The potential correlation between DES and statin or dyslipidemia | History of statin use or dyslipidemia is related to the increased probability of diagnosis of DES. | 172 | |
The heterozygous Ubiad1 G184R knock‐in mice | To study how UBIAD1 promotes the occurrence of SCD. | The Ubiad1 mutation associated with SCD impairs the transport of ER to Golgi apparatus, finally leads to accumulation of cholesterol in the cornea. | 173 | |
DR | The mice of ablation of Cyp46a1 | The role of CYP46A1 in retina and retinal vessels. | The ablation of Cyp46a1 leads to the increase of cholesterol in the retina and induce some manifestations of early DR. | 174 |
Abbreviations: AMD, age‐related macular degeneration; DES, dry eye syndrome; DR, diabetic retinopathy; LSS, lanosterol synthase; SCD, Schnyder corneal dystrophy; TSPO, 18‐kDa translocator protein.