Activated cGAS/STING signaling elicits endothelial cell senescence in early diabetic retinopathy.

Diabetic retinopathy (DR) is a leading cause of blindness in working-age adults and remains an important public health issue worldwide. Here we demonstrate that the expression of stimulator of interferon genes (STING) is increased in patients with DR and animal models of diabetic eye disease. STING has been previously shown to regulate cell senescence and inflammation, key contributors to the development and progression of DR.

Reducing Akt2 in retinal pigment epithelial cells causes a compensatory increase in Akt1 and attenuates diabetic retinopathy.

The retinal pigment epithelium (RPE) plays an important role in the development of diabetic retinopathy (DR), a leading cause of blindness worldwide. Here we set out to explore the role of Akt2 signaling-integral to both RPE homeostasis and glucose metabolism-to DR. Using human tissue and genetically manipulated mice (including RPE-specific conditional knockout (cKO) and knock-in (KI) mice), we investigate whether Akts in the RPE influences DR in models of diabetic eye disease.

Loss of interleukin-10 exacerbates early Type-1 diabetes-induced bone loss.

Type-1 diabetes (T1D) increases systemic inflammation, bone loss, and risk for bone fractures. Levels of the anti-inflammatory cytokine interleukin-10 (IL-10) are decreased in T1D, however their role in T1D-induced osteoporosis is unknown. To address this, diabetes was induced in male IL-10 knockout (KO) and wild-type (WT) mice.

Indocyanine green molecular angiography of choroidal neovascularization.

Retinal diseases such as proliferative diabetic retinopathy and neovascular AMD are characterized by the formation of new blood vessels. Current imaging techniques such as fluorescein and ICG angiography help to identify areas of vascular leakage but are limited in their applicability due to their nonspecific nature. However, as new treatment paradigms emerge in an effort to have patient specific treatments, the development of new imaging techniques that are capable of identifying patient specific biomarkers will become crucial for the success of these approaches.

Müller cells and diabetic retinopathy.

Müller cells are one of the primary glial cell types found in the retina and play a significant role in maintaining retinal function and health. Since Müller cells are the only cell type to span the entire width of the retina and have contact to almost every cell type in the retina they are uniquely positioned to perform a wide variety of functions necessary to maintaining retinal homeostasis. In the healthy retina, Müller cells recycle neurotransmitters, prevent glutamate toxicity, redistribute ions by spatial buffering, participate in the retinoid cycle, and regulate nutrient supplies by multiple mechanisms.

Modes of Retinal Cell Death in Diabetic Retinopathy.

Cell death seems to be a prominent feature in the progression of diabetic retinopathy. Several retinal cell types have been identified to undergo cell death in a diabetic environment. Most emphasis has been directed towards identifying apoptosis in the diabetic retina.