This paper provides a comprehensive analysis of the current state of intelligent ophthalmology in China, including technological advancements, academic exchange platforms, policy support, future challenges, and potential solutions. Technologically, remarkable progress have been made in various areas of intelligent ophthalmology in China, including diabetic retinopathy, fundus image analysis, and crucial aspects such as quality assessment of medical artificial intelligence products, clinical research methods, technological evaluation, and industrial standards. Researchers are constantly improving the safety and standardization of intelligent ophthalmology technology by formulating clinical application guidelines and standards. Academic exchange platforms have been established to provide extensive collaboration opportunities for professionals across diverse fields, and various academic journals serve as publication platforms for intelligent ophthalmology research. Regarding public policy, the Chinese government has not only established a supportive policy environment for the advancement of intelligent ophthalmology through various documents and regulations, but provided a legal basis and management framework. However, there are still challenges to overcome, such as technological innovation, data privacy and security, outdated regulations, and talent shortages. To tackle these issues, there is a requirement for increased technological research and development, the establishment of regulatory frameworks, talent cultivation, and greater awareness and acceptance of new technologies among patients. By comprehensively addressing these challenges, intelligent ophthalmology in China is expected to continue leading the industry's global development, bringing more innovation and convenience to the field of ophthalmic healthcare.

Objective : To explore the effects of inhibition of the inositol 1 , 4 , 5 ⁃trisphate receptor ( IP3R) ⅣCa2 + pathway on acetaminophen (APAP) Ⅳinduced liver injury in mice and its mitochondrial⁃associated endoplasmic reticulum membranes ( MAMs) . Methods : 40 SPF⁃rated male C57BL/6 mice were randomly divided into control group(n = 10) , model group( n = 10) , IP3R inhibitor(2⁃aminoethoxydiphenyl borate , 2 ⁃APB) group( n = 10) and the Ca2 + chelator [1 ,2 ⁃bis(2⁃aminophenoxy) ethane⁃N , N , N ′ N ′⁃tetraacetic acid , BAPTA⁃AM] group ( n = 10) . Mice in the model group ,2 ⁃APB group , and BAPTA⁃AM group were given a single intraperitoneal injection of APAP (300 mg/kg) . Half an hour before APAP injection , mice in the 2 ⁃APB group were injected intraperitoneally with 2 ⁃ APB(20 mg/kg) and mice in the BAPTA⁃AM group were injected intraperitoneally with BAPTA⁃AM(2. 5 mg/ kg) . The mice in each group were executed 24 hours after intraperitoneal injection of APAP. Serum alanine aminotransferase (ALT) and aspartate aminotransferase ( AST) were measured by chemical method. The pathological change of liver was observed by HE staining. The ultrastructural changes of mitochondria , endoplasmic reticulum and MAMs in liver cells were observed by transmission electron microscopy. The changes of Ca2 + in liver tissue homogenate were measured by calcium assay kit. The protein expression levels of mitofusin 1 ( MFN1 ) , mitofusin 2 (MFN2) , inositol 1 ,4 ,5 ⁃trisphate receptor(IP3R1) ,glucose regulated protein 75(GRP75) were detected by Western blot. Results : Compared with the control group , the serum ALT and AST in the model group increased (P <0. 01) . Disorganized hepatocyte arrangement , hepatocyte degeneration and lobular central necrosis were observed. Breakage and disappearance of mitochondrial cristae , swelling and fracture of the endoplasmic reticulum and increase of the number of MAMs were also observed by transmission electron microscopy. The Ca2 + level in liver tissue homogenate increased ( P < 0. 01) . MFN1 and MFN2 protein expression decreased ( P < 0. 01) , IP3R1 and GRP75 protein expression increased( P < 0. 01) . Compared with the model group , the serum ALT and AST in 2 ⁃APB group and BAPTA⁃AM group decreased ( P < 0. 01 ) , the liver pathological changes were significantly improved , MAMs decreased , the content of Ca2 + in liver homogenate decreased(P < 0. 01) , MFN1 and MFN2 protein expression increased(P < 0. 01) , IP3R1 and GRP75 protein expression decreased(P < 0. 01) . Conclusion Inhibition of the IP3R⁃Ca2 + pathway protects against APAP⁃induced liver injury in mice. Its mechanism is related to reducing hepatic Ca2 + levels , reducing the number of MAMs , and regulating the expression of MAMs⁃related proteins.