- Written by Super User
- Category: March 2021: Issue 1(12)
- Published: 05 April 2021
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https://doi.org/10.30702/Ophthalmology31032021-12.1.122-131/112.5
UDC 617.7-007.681:617.735:617.731:577.112.5
Lutsenko N. S.1, Nedilka T. V.2
1Zaporizhia Medical Academy of Post-graduate Education of the Ministry of Health of Ukraine, Zaporizhzhia, Ukraine
2“Zaporizhzhia Regional Clinical Hospital” of the Zaporizhzhia Regional Council, Zaporizhzhia, Ukraine
Abstract. Heat shock proteins (HSP) are important components of the defense mechanism that increases the survival of body cells in adverse conditions due to antiapoptotic and cytoprotective effects. Since their discovery, numerous studies and experimental models have proved the role of HSPs as a key link in the processes of both repair and coagulation of proteins, as well as in the protection of cells from oxidative stress. The potential for pharmacological induction of HSPs in the human body makes them an attractive therapeutic target for many neurodegenerative diseases. This review examines the role of HSPs, especially fraction 70, in the mechanisms of neuroprotection of retinal ganglion cells in primary open-angle glaucoma being one of the common neurodegenerative diseases that can lead to complete loss of visual functions. A number of studies have shown the protective effect of HSP70 on retinal ganglion cells in animals with artificially induced glaucoma. But in the course of experiments on animal models, it was also proved that direct immunization with HSP through intravitreal injections induced pressure-independent degeneration of retinal ganglion cells. This indicates the need for indirect stimulation of HSP70 in order to activate their neuroprotective properties. To date, there are insufficient data on the circulation of HSP70 in the body of a person with glaucoma. These data indicate the prospects for further study of the role of HSP70 in glaucoma degeneration and elucidation of the ways of their mediated induction.
Keywords: heat shock protein, HSP70, glaucoma, ganglion cells, retina, neuroprotection.