Illustration depicting<unk> <unk>  is the result of damage to the small blood vessels and neurons of the retina. The earliest changes leading to<unk>  include narrowing of the retinal arteries associated with reduced retinal blood flow; dysfunction of the neurons of the inner retina, followed in later stages by changes in the function of the outer retina, associated with subtle changes in visual function; dysfunction of the blood-retinal barrier, which protects the retina from many substances in the blood (including toxins and immune cells), leading to the leaking of blood constituents into the retinal neuropile. Later, the basement membrane of the retinal blood vessels thickens, capillaries degenerate and lose cells, particularly pericytes and vascular smooth muscle cells. This leads to loss of blood flow and progressive ischemia, and microscopic aneurysms which appear as balloon-like structures jutting out from the capillary walls, which recruit inflammatory cells; and advanced dysfunction and degeneration of the neurons and glial cells of the retina. The condition typically develops about 10–15 years after receiving the diagnosis of diabetes mellitus. An experimental study suggests that pericyte death is caused by blood glucose persistently activating protein kinase C and mitogen-activated protein kinase (MAPK), which, through a series of intermediates, inhibits signaling through platelet-derived growth factor receptors — signaling that supports cellular survival, proliferation, and growth. The resulting withdrawal of this signaling leads to the programmed cell death (apoptosis) of the cells in this experimental model. In addition, excessive sorbitol in<unk> s is deposited on retina tissue and it is also proposed to play a role in<unk> . Small blood vessels – such as those in the eye – are especially vulnerable to poor blood sugar (blood glucose) control. An overaccumulation of glucose damages the tiny blood vessels in the retina. During the initial stage, called nonproliferative<unk>  (NPDR), most people do not notice any change in their vision. Early changes that are reversible and do not threaten central vision are sometimes termed background retinopathy. A genetic study showed that<unk>  shares a similar genetic predisposition with levels of glucose, low-density lipoprotein cholesterol, and systolic blood pressure, indicating that glycemic control and cardiometabolic factors may be important in the development of<unk> . Some people develop a condition called macular edema. It occurs when the damaged blood vessels leak fluid and lipids onto the macula, the part of the retina that lets us see detail. The fluid makes the macula swell, which blurs vision. Proliferative<unk>  === As the disease progresses, severe nonproliferative<unk>  enters an advanced or proliferative (PDR) stage, where blood vessels proliferate/grow. The lack of oxygen in the retina causes formation of new fragile blood vessels to grow along the retina and in the clear, gel-like vitreous humour that fills the inside of the eye. Without timely treatment, these new blood vessels can bleed and cause cloudy vision, and destroy the retina. Fibrovascular proliferation can also cause tractional retinal detachment. The new blood vessels can also grow into the angle of the anterior chamber of the eye and cause neovascular glaucoma. Nonproliferative<unk>  shows up as cotton wool spots, or microvascular abnormalities or as superficial retinal hemorrhages. Even so, the advanced proliferative<unk>  (PDR) can remain asymptomatic for a very long time, and so should be monitored closely with regular checkups.
Diabetic retinopathy
Autoimmune retinopathy
Hypertensive retinopathy
Radiation retinopathy
Photic retinopathy
Retinal vasculitis
Autoimmune optic neuropathy
Sickle cell retinopathy