Diabetic Cataract Pathological Research Services
The pathogenesis of diabetic cataract is complex and involves multiple pathophysiological processes. Accurately analyzing these pathologic mechanisms is the core prerequisite for the development of early prevention and treatment. Ace Therapeutics provides global pharmaceutical companies and research institutions with comprehensive pathology research services from model construction to mechanism validation. We are committed to advancing the understanding of diabetic cataract pathogenesis through multidisciplinary technologies, which will provide a scientific basis for innovative drug discovery and diagnostic technology development.
Pathogenesis of Diabetic Cataracts
Different types of mechanisms have been proposed for the pathogenesis of cataract in cases of DM.
The overactivation of aldose reductase (AR) leads to sorbitol accumulation, causing swelling and rupture of lens fiber cells, ultimately resulting in degeneration and cataract formation.
- Osmotic and oxidative stress
Hyperglycemia may lead to auto-oxidation of glucose and non-enzymatic glycation, collectively referred to as glycoxidation, resulting in the overproduction of free oxygen radicals in the lens. Superoxide dismutase (SOD) activity is decreased, and oxidation products such as malondialdehyde (MDA) damage epithelial cell DNA.
- AGEs-RAGE signaling pathway
Late glycosylation end products (AGEs) bind to the lens receptor RAGE and activate the p38 MAPK pathway to induce interstitial fibrosis.
In recent years, the molecular level regulation and pathological processes of lens epithelial cells (LECs) have also been shown to play a role in the development of DC. In addition, epigenetic regulations, include lncRNA, circRNA, microRNA, methylation of RNA and DNA, histone acetylation and pathological processes, include autophagy, fibrosis and apoptosis of LECs also involved in DC. Therefore, a comprehensive understanding and elucidation of how chronic hyperglycemia drives molecular-level regulations and cytopathological processes in the lens will shed lights on the prevention, delay and treatment of DC.
Fig. 1 Pathways for AGEs formation under the condition of high glucose. (Guo Z., et al., 2023)
Our Diabetic Cataract Pathological Research Services
Ace Therapeutics provides a one-stop solution for diabetic cataract pathology research. We integrate advanced model resources with multidimensional technologies and analytical approaches, dedicated to systematically elucidating the distinct mechanisms of lens opacification under hyperglycemic conditions, thereby offering scientific support for clients' target discovery, drug screening, and translational research.
Diabetic Cataract Research Modeling Service
- Animal modeling and validation services
We offer animal models that can be used to study the pathology of diabetic cataracts.
| Animal Models |
Features |
| Induction models |
Type 1 diabetes model |
STZ selectively destroys pancreatic β-cells, mimicking the hyperglycemic state of type 1 diabetes, secondary to oxidative damage and clouding of the lens. |
| Type 2 diabetes model |
High-fat diet combined with low-dose STZ mice (simultaneous presentation of insulin resistance and oxidative stress phenotypes). |
| Genetic engineering models |
RAGE overexpression mouse model |
Abnormally high expression of RAGE in a simulated diabetic state to trigger cataract pathological phenotypic features. |
We offer the following diabetic cataract animal model validation services.
- Dynamically monitor the degree of lens opacification using a slit-lamp microscope.
- Observe lens fiber cell vacuolization and epithelial cell apoptosis via HE staining of eyeball tissues.
- Detect AGEs deposition sites through immunohistochemical analysis.
- Measure oxidative stress indices such as superoxide dismutase (SOD) and malondialdehyde (MDA).
- Cellular Models and Organoid Platforms
| Models |
Features |
| Human Lens Epithelial Cell (HLE-B3) Diabetes Model |
- We provide high glucose-treated cell models that mimic the diabetic microenvironment and support oxidative stress, apoptosis, and epithelial-mesenchymal transition (EMT) marker assays.
- Advanced service: 3D lens organoid culture, in which HLE-B3 cells are wrapped in matrix gel to form spheroids, which can more realistically reflect the differentiation and clouding process of lens fiber cells.
|
Research Service on the Pathogenesis of Diabetic Cataracts
We provide specialized diabetic cataract pathology research services dedicated to unraveling the unique molecular mechanisms and pathological processes of lens clouding in a hyperglycemic environment. For this complex ocular disease, which is highly associated with diabetes progression, our research services encompass:
- Molecular Mechanisms: In-depth analysis of hyperglycemia-induced polyol pathway abnormalities, increased oxidative stress, accumulation of advanced glycosylation end-products (AGEs), protein kinase activation and other core pathological mechanisms in lens epithelial cells and fibroblasts.
- Cell Biology Studies: To assess the alterations in key biological behaviors of lens epithelial cells such as proliferation, migration, apoptosis, autophagy, and epithelial-mesenchymal transition (EMT) under diabetic conditions and their impact on lens transparency.
- Histopathological analysis: Using histological staining (e.g., HE), special staining (e.g., PAS), immunohistochemistry/immunofluorescence, etc., we can accurately locate and quantify the expression of key proteins, infiltration of inflammatory factors, the degree of fibrosis, and other pathological features in the lens tissue.
- Signaling pathway analysis: To systematically study the role of MAPK, PI3K/Akt, NF-κB, Nrf2/ARE, TGF-β and other signaling pathways in the development of diabetic cataracts and their interactive regulatory networks.
Our Advanced Technology Platforms
| Technologies |
Applications |
| DCFH-DA fluorescent probe combined flow cytometry / Confocal microscopy |
Quantification of intracellular oxidation levels in the lens. |
| ELISA assay |
Measurement of AGEs in ocular tissues/cells. |
| Immunofluorescence |
Localization of AGEs deposition in lens fibers. |
| Western blot |
Detection of glycation modifications of lens proteins (e.g., β-crystallin) |
| Phosphorylated protein antibody microarray high-throughput detection combined with qPCR validation analysis |
In-depth analysis of diabetic cataract-related signaling pathways and validation of key gene (e.g., IL-6, TNF-α, HO-1) expression. |
| Lens tissue RNA-seq |
Screening for differentially expressed genes (DEGs) under hyperglycemic treatment, with enrichment analysis targeting pathways such as 'protein folding,' 'redox processes,' and 'extracellular matrix organization. |
| Lens proteomics (Label-free/iTRAQ) |
Detection of changes in lens protein expression and post-translational modifications (phosphorylation, glycosylation). |
| Targeted metabolomics |
Detection of polyol pathway metabolites such as glucose, sorbitol, and inositol in lens tissue. |
Advantages of Our Diabetic Cataract Pathological Research Services
- Multidimensional Integrated Research: Combining molecular, cellular, and tissue levels to provide comprehensive and systematic pathological research services.
- Facilitating drug target discovery: Providing a robust scientific foundation for developing preventive and therapeutic strategies that target the distinct pathological mechanisms of diabetic cataracts.
- Customized services: We can design and implement a customized research plan based on your specific research needs.
Ace Therapeutics provides a one-stop solution from basic model construction to in-depth mechanism analysis. Contact us today for a customized solution and let us be your key partner in diabetic cataract research.
References
- Guo Z, Ma X, Zhang R X, et al. Oxidative stress, epigenetic regulation and pathological processes of lens epithelial cells underlying diabetic cataract. Advances in ophthalmology practice and research. 2023, 3(4): 180-186.
- Kiziltoprak H, Tekin K, Inanc M, et al. Cataract in diabetes mellitus. World journal of diabetes. 2019, 10(3): 140.
All of our services and
products are intended for preclinical research use only and cannot be used to diagnose, treat or
manage patients.
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