**1. Introduction**

The term "Glaucoma" integrates a wide range of eye diseases characterized by a diversity of clinical forms: mainly by the chronic course and rather unfavourable prognosis. Sufficient to mention that in developed countries the frequency of vision loss due to glaucoma is steadily at the level of 15-20% of the total number of all blind subjects [*Nesterov A.P., 2008*].

It is considered long-established that among various clinical-and-anatomical manifestations of the glaucomatous process the anterior open-angle glaucoma is the most frequently diag‐ nosed form.

The severity of course of anterior open-angle glaucoma and especially the unfavourable outcomes of the disease are mainly connected with those unsolvable problems faced by ophthalmologists at the study of pathogenesis of primary and secondary glaucomas. Precisely this circumstance is the "insurmountable" obstacle in pathogenetic therapy, thus limiting the entire complex of medical interventions within the early symptomatic therapy with underlying local application of hypotensive means aimed to decrease intraocular pressure.

To a known extent, the interpretation of aspects of pathogenesis in case of anterior open-angle glaucoma is connected to the fact that this type of glaucoma is rather frequently associated with the cataract and pseudoexfoliative syndrome.

At present the etiopathogenetic links engaged in induction and the course of anterior openangle glaucoma are conditionally divided into general and local ones.

© 2013 Zilfyan; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Heredity, general type changes in specific integrative systems of the organism (CNS, endo‐ crine, immune and cardiovascular) are among the general factors bringing forth disorders of the hematoophthalmic barrier and the increase of intraocular pressure.

To our mind, during the last years rather informative data signifying in favour of pleotropic

Modern Aspects of Glaucoma Pathogenesis Local Factors for Development of Primary Open-Angle Glaucoma…

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In particular, in a post-surgery period in patients operated for complicated and senile cataracts *in situ* produced TGFβ-2 induces trans-differentiation of epithelial cells of crystalline lens capsule into fibroblasts; this latter was manifested as opacity of lens with all the subsequent after-effects [*Dawes L.J. et al., 2009*]. The modulatory effect of TGFβ-1 towards the processes of activation of cells of fibroblastic line in the cornea was also established. Thus, the authors [*Karamichos D. et al., 2010*] under conditions of cultivating cells of cornea using TGFβ-1 dosedependent mode activated *in situ* synthetic processes in fibroblasts, thus bringing forth intensification of collagen(ous) fibrilles synthesis and eventually to regional overgrowth of

TGFβ-2 high level was also revealed in cells of the trabecular meshwork of patients with openangle glaucoma [*Stefan C. et al., 2008*]. The authors consider that at the mentioned disease TGFβ-2 stimulates fibronectin synthesis in trabecular cells, thus predefining "profibrotic"

Literature data is available [*Ochiai Y., Ochiai H., 2002*], according to which in patients with anterior open-angle glaucoma, diabetes complicated by anterior open-angle glaucoma the level of TGFβ-2 in aqueous / intraocular humor is markedly increased. As a control, the authors

Processes reflecting the specific precise stages of TGFβ-2 and IGF-1 activity in post-barrier membranes of the eye are the subject of a wide discussion. Furthermore, the study on mech‐ anisms of their direct and/or mediated interaction in processes ensuring the drainage function

In the organism of mammals, the post-barrier membranes of an eye also serve as a source of both cytocines. IGF-1 and its receptors, IGF-IR, were found in epitheliocytes of lens and cornea, epitheliocytes of retina meshwork, Muller's cells [*Shaw L.C. et al., 2006; Ko J.A. et al., 2009*]. TGFβ-2 is produced in post-barrier membranes of an eye and, first of all, in fibroblasts of cornea [*Streilein J. et al., 1992; Wilkbanks G. et al., 1992; Hollborn M. et al., 2000; Fleenor D. et al., 2006*].

According to C. Stefan et al. (2008), cells of the trabecular meshwork of the anterior angle of

S.H. Chung and associates used human lens epithelial cells (HLE B-3) to reveal the role of IGF-1 in processes of TGFβ-2 mediated fibronectin accumulation in lens cells [*Chung S.H. et al., 2007*]. Based on analysis performed by the authors (reverse polymerase transcriptase chain reaction, immune-fluorescent studies) mentioned researchers draw a conclusion that IGF-1 counteracts

J.A. Ko et al. (2009) studied the role of IGF-1 in intrercellular regulation in cultured fibroblasts and human corneal epitheliocytes. According to authors, the presence of epitheliocytes in the culture medium enhanced N-cadherin expression in fibroblasts. Similar effect of corneal epitheliocytes was also simulated by IGF-1, but not fibroblasts growth factor or epidermal

potencies of TGFβ-2 produced in post-barrier membranes of the eye.

immature connective tissue with the resulting fibrosis.

effects of TGFβ-2 in post-barrier membranes of the eye.

studied aqueous humour of patients with cataracts.

the eye chamber might serve as the source of TGFβ-2 synthesis.

TGFβ-2 induced fibronectin accumulation in lens epitheliocytes.

of an eye is mainly emphasized.

Amongst the local factors relatively persistent elevation of intraocular pressure, primary dystrophic and atrophic changes, including age-related shifts in the cornea, ciliary body and the trabecular meshwork, which cause the infringement of hydrodynamic and hydrostatic properties of the aqueous humour, are considered.

As mentioned by A.P. Nesterov (2008) chronologically occurring processes, which might be conditionally subdivided into 2 stages, are engaged in the pathogenesis of glaucomas in anterior and posterior chambers of an eye. At the first stage mechanisms bringing forth the increase of intraocular pressure are triggered in the anterior chamber of an eye. At the second stage mechanisms localized in the posterior part of the eye chamber are initiated and in the long run become the cause of atrophy of the visual nerve. At that, the "glaucomatous process" firstly originates in the anterior chamber of an eye, while the dystrophic and atrophic processes in the visual nerve are resulting from the exposure to high intraocular pressure.

During the last years, rather informative evidences were obtained to discuss the role of biologically active substances produced *in situ*, i.e. in specific eye membranes, in mechanisms of anterior open-angle glaucoma origination using the clinical and experimental material.

We did not set the problem to analyze the current state of the art on the role of general pathogenetic factors engaged in induction and the course of anterior open-angle glaucoma.

The currently available data of scientific publications and results of our own investigations devoted to the role of *in situ* produced biologically active substances of cytokine, mediatory and hormonal origin in mechanisms of a stable increase of the intraocular pressure in case of anterior open-angle glaucoma will be analyzed in this work.
