Pathogenesis of diabetic retinopathy

Retina image

Currently, the pathogenesis of diabetic retinopathy is linked with retinal hypoxia, vascular damage, etc.

  1. Thickening of and damage to retinal capillary walls.
  2. Loss of pericytes of capillaries.
  3. Breakdown of the blood-retinal barrier.

The interpretation of the pathogenesis of diabetic retinopathy developed by me, Professor R. V. Hajiyev

  1. Damage to retinal glial cells (Mueller cells)
  2. Breakdown of the extracellular matrix.
  3. Thickening of and damage to the capillary membrane.
  4. Breakdown of the blood-retinal barrier.

Scheme of the development of diabetic retinopathy

Normally, when light falls on the retina, rhodopsin in the outer layers of the photoreceptor splits. Rhodopsin is a complex protein consisting of two parts of the retinal (mono11 cis aldehyde carotene A) and opsin. When rhodopsin splits, it breaks down into a number of intermediate products: prelumirhodopsin, lumirhodopsin, metarhodopsin I, metarhodopsin II, etc.

At this moment, a lot of energy and toxic products are released. It is believed that they are released at the stage of transition from metarhodopsin I to metarhodopsin II. Toxic products are very active and can destroy cell membranes. But normally, this does not happen, because they are neutralized by antioxidant system of the pigment epithelium, which covers the photoreceptors.

That is why photoreceptors are recessed into the layer pigment epithelium. The layer of choriocapillaries is a kind of radiator that drains the resulting excess heat.


If there are too many toxic products, they penetrate into the inner layers of the retina and enter the vitreous body, where they are neutralized by the enzymatic system of the vitreous body. We have indicated the high activity of glutathione peroxidase in the vitreous body.

What happens in diabetes? In diabetes, a much greater amount of toxic products form because of the slow breakdown of all types of metabolism, especially lipid. So it is much more difficult for the retina to cope with this pressure.

Toxic products penetrate into the inner layers of the retina and the first cells they encounter are the Mueller glial cells. Bipolar cells are not affected because they are an extension of the photoreceptors, which form, together with them and glial cells, the main conglomerate protected by the photoreceptors — retinal pigment epithelium.

Mueller cells are left unprotected. It is known from neuroscience that the main function of glia is a nutritional function. Nerve cells receive nutrients from the blood vessels not directly, but through the glia. This is logical, because it protects the nerve cells during food poisoning.

Histological studies conducted by me with experimental diabetes in rabbits have shown that glial cells are damaged in experimental diabetes (amido black colour 10B)

Retina glia is like bedding for retinal vessels and, of course, when damaged, it cannot but cause damage to the surrounding blood vessels.

Glial cells begin in the inner plexiform layer and contain a yellow pigment. So, apparently, hard exudates result not from the transudation of lipids through the vascular wall but from the outer portion atrophy of the Mueller cells.

Naturally, where there are «hard exudates», there is increased vascular permeability there.

In the future, non-neutralized and free radicals penetrate into the deeper layers of the retina and can disrupt contacts between fibrils of the vitreous body and Mueller cells in the membrane limiting interna. In fact, it is not a membrane, but processes of Mueller cells turning into vitreous fibrils. The place of contact is disrupted, and there can be posterior vitreous detachment.

Posterior vitreous detachment is an extremely unfavourable factor stimulating the development of diabetic retinopathy. This may occur because the retina at that location loses contact with the vitreous antioxidant system. I indicated for the first time that the vitreous body contains a high activity of glutathione peroxidase, and based on a milligram of protein, it is much higher than in the surrounding tissues. It is this system that helps the retina to neutralize toxic products.

Thus, the pathogenesis of diabetic retinopathy is based on primary damage to Mueller cells. But since it is impossible for one damaged tissue in the body not to affect surrounding tissues, damage affects complex glial cells, the extracellular matrix and blood vessels.

However, despite the mechanism of the development of diabetic retinopathy we have described (which we think is correct), the basis of these processes is inflammation.

Mueller cells are connective tissue cells. We know from histology that all inflammatory processes occur in connective cells. It is these cells that are the scene of battles between microbes. Hence, diabetic retinopathy is a kind of inflammatory process that develops only in the presence of diabetes.

Therefore, patients with diabetes often develop other inflammatory processes: sluggish uveitis leading to rear adhesions and symptoms of the narrow pupil. In some cases, this symptom makes the extraction of cataract in diabetes difficult. There is a drift between these states (the conjunctiva, vascular membrane and retina).

What is it? The new HAT medicine system responds to this.


We noticed that the progression of diabetic retinopathy in some patients was accompanied by a decrease in back pain.

We had several attempts to treat diabetic retinopathy similar to the treatment of optic nerve atrophy. In the treatment of optic nerve atrophy, we take a bacteriological analysis of the conjunctiva of the eye and restore the immunological balance. It is precisely the imbalance between the microbial flora of the conjunctiva and the antibodies in some cases that causes chronic conjunctivitis and atrophy of the optic nerve in others. The restoration of this balance is accompanied by the improvement of vision.

In the treatment of diabetic retinopathy in this way, there was deterioration accompanied by an increase in the amount of bleeding and decreased vision.

Thus, the progression of diabetic retinopathy is apparently due not to the eye, but to another attractor. What attractor it is remains a question for us.


  1. Hajiyev R.V. Diabetic retinopathy, Baku, «Elm», 1999, p. 71.
  2. Gajiyev Posterior vitreous detachment in pathogenesis of diabitic retinopathy. Ophthalmosurgery (ISSN 0235-4160), 1992, 2, p.48-52
  3. Sultanov M. Yu., Gadjiev R.V. Asymmetry of the diabetic involvemetn of the retina in miopia. Vestnik ofthalmologii, 1990, 1, 106, p. 49-51
  4. Gadzhiyev R.V. Contibution of the ocular shape and size to the course of diabetic retinopathy. Vestnik oftalmologii 1994, 4, 110, p. 10-12
  5. Aliyeva Z.A., Gadzhiev R.V., Sultanov M.Y. About the passible role of antioxidant system of the vitreous body delayed development of diabitic retinopathy. Oftalmologiceskiy journal 1985, 3, p. 142-145.
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