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Experimental drug shows potential in preventing or slowing Diabetic eye disease, Study finds

A recent study conducted by researchers, including an Indian-origin scientist, has provided promising evidence that an experimental drug could potentially aid in preventing or slowing down vision loss among individuals with diabetes.

The findings, which have been published in the Journal of Clinical Investigation, stem from a comprehensive investigation utilizing mouse models, human retinal organoids, and eye cell lines.

The research was primarily conducted by the team at the Wilmer Eye Institute, Johns Hopkins Medicine, with a specific focus on two prevalent diabetic eye conditions: proliferative diabetic retinopathy and diabetic macular edema.

Both of these conditions directly impact the retina, which serves as the light-sensing tissue located at the back of the eye and is responsible for transmitting visual signals to the brain.

In proliferative diabetic retinopathy, abnormal blood vessels excessively grow on the surface of the retina, leading to bleeding, retinal detachments, and severe vision impairment.

Diabetic macular edema, on the other hand, involves the leakage of fluid from blood vessels in the eye, causing swelling in the central retina and damaging the retinal cells responsible for central vision.

The study revealed that a specific compound known as 32-134D displayed potential in preventing diabetic retinal vascular diseases by reducing the levels of a protein called HIF, or hypoxia-inducible factor.

"Our findings demonstrated that 32-134D was remarkably well-tolerated when applied to the eyes and effectively reduced HIF levels in diseased eyes," stated Dr. Akrit Sodhi, Associate Professor of Ophthalmology at Johns Hopkins and the Wilmer Eye Institute.

To evaluate the efficacy of 32-134D, the researchers administered the compound to various types of human retinal cell lines associated with the expression of proteins that promote blood vessel production and leakage.

Upon analyzing the genes regulated by HIF in cells treated with 32-134D, the researchers observed a return to near-normal levels of gene expression.

This outcome proved sufficient in halting the formation of new blood vessels and maintaining the structural integrity of existing vessels.

Furthermore, the researchers tested 32-134D in two distinct mouse models of diabetic eye disease by administering injections directly into the eye. After five days, they observed reduced levels of HIF and noted that the drug effectively hindered the formation of new blood vessels and prevented vessel leakage.

Consequently, this slowed down the progression of the eye disease in the animal models.

Dr. Sodhi and his team were pleasantly surprised to discover that 32-134D remained active in the retina for approximately 12 days following a single injection, without causing harm to retinal cells or tissue degradation.

"This research highlights the potential of inhibiting HIF with 32-134D as not only an effective therapeutic approach but also a safe one," emphasized Dr. Sodhi, while emphasizing the need for further animal model studies before advancing to clinical trials. (Edited)

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