Diabetes has become a leading cause of death worldwide. Although there is no cure for diabetes, blood glucose monitoring combined with appropriate medication can enhance treatment efficiency, alleviate the symptoms, as well as diminish the complications. For point-of-care purposes, continuous glucose monitoring (CGM) devices are considered to be the best candidates for diabetes therapy. This review focuses on current growth areas of CGM technologies, specifically focusing on subcutaneous implantable electrochemical glucose sensors. The superiority of CGM systems is introduced firstly, and then the strategies for fabrication of minimally-invasive and non-invasive CGM biosensors are discussed, respectively. Finally, we briefly outline the current status and future perspective for CGM systems.

Patients of diabetes mellitus urgently need noninvasive and continuous glucose monitoring in daily point-of-care. As the tear glucose concentration has a positive correlation with that in blood, the hydrogel colloidal crystal integrated into contact lens possesses promising potential for noninvasive monitoring of glucose in tears. This paper presents a new glucose-responsive sensor, which consists a crystalline colloidal array (CCA) embedded in hydrogel matrix, attached onto a rigid gas permeable (RGP) contact lens. This novel sensing lens is able to selectively diffract visible light, whose wavelength shifts between 567 and 468 nm according to the alternation of the glucose concentration between 0 and 50 mM and its visible color change between reddish yellow, green, and blue. The detection limit of responsive glucose concentration can be reduced to 0.05 mM. Its combination with a contact lens endows it with excellent biocompatibility and portability, which shows great possibility for it to push the development of glucose-detecting devices into new era.

Scleral extracellular matrix (ECM) remodeling is thought to play a critical role in the pathogenesis of glaucoma. Mechanical strain induced by elevated intraocular pressure can promote myofibroblast differentiation of fibroblasts and result in scleral ECM remodeling; however, the underlying mechanism remains poorly understood. Yes-associated protein (YAP) is a mechanosensory protein and the key downstream transcriptional effector of the Hippo signaling pathway. Here, we investigated the role of YAP in mechanical strain-induced myofibroblast transformation during glaucoma scleral ECM remodeling. Integrative bioinformatics analyses were performed to identify the key pathways for the ECM remodeling of the sclera in glaucoma. Sprague–Dawley rats were used to establish a chronic ocular hypertension model, and the expression of collagen type I (COL1) and YAP in the sclera was analyzed by immunohistochemical analysis and Western blotting. Furthermore, human scleral fibroblasts (HSFs) were cultured and subjected to mechanical strain. In groups with or without the YAP siRNA or YAP inhibitor, cell proliferation, migration capacity, and the expression levels of YAP, COL1, and α-smooth muscle actin (α-SMA) were evaluated by Cell Counting Kit-8 assay, scratch assay, and Western blotting. The interactions between YAP and Smad3 were demonstrated by coimmunoprecipitation, and the expression levels of COL1 and α-SMA were evaluated in groups treated with or without the Smad3 inhibitor. We first revealed that the Hippo signaling pathway may be involved in mechanical strain-induced scleral ECM remodeling through bioinformatics analysis. Furthermore, the in vivo study showed upregulated YAP, COL1, and α-SMA expression in the hypertensive sclera of rats. In vitro, mechanical strain increased YAP and COL1 expression in HSFs and promoted myofibroblast differentiation. After YAP knockdown or inhibition with verteporfin, mechanical strain-induced fibrotic changes in HSFs were markedly suppressed. Additionally, YAP showed a protein interaction with Smad3, and the upregulation of a-SMA and COL1 in response to mechanical strain was also significantly downregulated following the inhibition of Smad3. In conclusion, mechanical strain activated scleral myofibroblast differentiation via YAP. The YAP pathway may play an important role in regulating scleral myofibroblast differentiation and ECM remodeling of the sclera in glaucoma.

To identify whether myopia was associated with the visual field (VF) progression of primary open-angle glaucoma (POAG). A total of 270 eyes of 270 POAG followed up for more than 3 years with ≥9 reliable VFs by Octopus perimetry were retrospectively reviewed. Myopia was divided into: mild myopia (-2.99 diopter [D], 0), moderate myopia (-5.99, 3.00 D), marked myopia (-9.00, -6.00 D) and non-myopia (0 D or more). An annual change in the mean defect (MD) slope >0.22 dB/y and 0.30 dB/y was defined as fast progression, respectively. Logistic regression was performed to determine prognostic factors for VF progression. For the cutoff threshold at 0.22 dB/y, logistic regression showed that vertical cup-to-disk ratio (VCDR; p = 0.004) and the extent of myopia (p = 0.002) were statistically significant. When logistic regression was repeated after excluding the extent of myopia, axial length (AL; p = 0.008, odds ratio [OR] = 0.796) reached significance, as did VCDR (p = 0.001). Compared to eyes with AL≤23 mm, the OR values were 0.334 (p = 0.059), 0.309 (p = 0.044), 0.266 (p = 0.019), 0.260 (p = 0.018), respectively, for 23 <AL≤24 mm, 24 <AL≤25 mm, 25 26 mm. The significance of vertical cup-to-disk ratio of (p = 0.004) and the extent of myopia (p = 0.008) did not change for the cutoff threshold at 0.30dB/y. VCDR and myopia were associated with VF prognosis of POAG. Axial myopia may be a protective factor against VF progression.

Background: Glaucoma is a leading cause of irreversible blindness. Remodeling of the scleral extracellular matrix (ECM) plays an important role in the development of glaucoma. The aim of this study was to identify the key genes and pathways for the ECM remodeling of sclera in glaucoma by bioinformatics analysis and to explore potential therapeutic agents for glaucoma management.