Diabetic Macular Edema Drug Discovery Service

With many years of experience, Creative Biolabs has become a leading company in the field of biological research, whether through classical bioanalytical methods or more advanced and complex approaches, we offer one-stop solutions for diabetic macular edema (DME) corresponding services and provide stable, reproducible data profiles.

Background of DME

DME is a diabetic complication caused by chronic damage to the neurovascular structure of the retina. About 75 percent of people with type 1 diabetes and half of the people with type 2 diabetes develop retinopathy, which is the leading cause of visual impairment and blindness. Systemic factors associated with DME include a long history of diabetes, high systolic blood pressure and high hemoglobin, and ocular factors associated with DME are mostly the severity of diabetic retinopathy (DR).

Pathology of DME

Research in the past few years has confirmed that almost all types of retinal cells are damaged by diabetes, and the biological definition of DR and DME also includes almost all retinal functions and structural changes such as neurons, Muller cells, and astrocytes. It is well known that the etiology of DME is closely related to the diabetes process itself, but the exact mechanisms that initiate and lead to retinal damage and visual impairment remain to be elucidated.

Fig 1. Pathways that may be involved in the DME process. (Romero-Aroca, 2016)

One pathological explanation of DME is the oxygen theory, that prolonged hyperglycemia leads to a decrease in intraretinal oxygen tension and triggers an autoregulatory response in retinal arterioles, which in turn leads to increased hydrostatic pressure on intraretinal capillaries and damages them. Another pathological explanation for DME comes from chronic inflammation caused by diabetes. This is theoretically supported by cellular phenomena such as cellular edema, microglial activation, and leukocyte arrest.

Therapeutic Approaches for DME

Clinically, DR is diagnosed by observing bleeding and microaneurysms by means of fundus photography and fluorescein angiography. The prevention and treatment of DME are mainly carried out by strictly controlling blood sugar and blood pressure. The current standard of intervention for DME is pan-retinal photocoagulation, a technique that can reduce the risk of vision loss in patients greatly. In addition, focal macular laser photocoagulation is also an optional surgical method.

Fig 2. Color photograph, fluorescein angiography and optical coherence tomography of the right eye of a patient with DME. (Rashaed, 2013)

With the in-depth understanding of the mechanism of DME and diabetes, some drugs and molecular treatments have also entered the candidate list. Currently, the most promising drugs are anti-vascular endothelial growth factor (VEGF) drugs. Diabetes increases the secretion of VEGF and leads to an increase in vascular permeability and angiogenesis, so blocking VEGF molecules has become the focus of controlling DME symptoms. In addition, the development of advanced glycation end-product blockers and vitreous-promoting enzymes has provided more options for preventing or even reversing DME symptoms.

Our Services

• In Vitro Services
• In Vivo Services
• Ex Vivo Services
• Discovery Services
• Development Services

Thanks to our professional R&D team, Creative Biolabs will carefully evaluate and plan each stage, whether at the tissue level or more molecular level, we can study not only upstream metabolic pathways, but also downstream symptoms and consequences. If you want to deepen your understanding of the mechanism of DME or are working to develop better ways to maintain vision, we can be your most reliable partner. Please feel free to contact us with our specialist for further information.

References

1. Romero-Aroca, P.; et al. Diabetic macular edema pathophysiology: Vasogenic versus inflammatory. Journal of Diabetes Research. 2016, 10: 2156273.
2. Rashaed, S.A.; et al. Combined therapy for diabetic macular edema. Middle East African Journal of Ophthalmology. 2013, 20(4): 315-320.