Abstract

The study of the pathogenesis of retinopathy of prematurity (ROP) is the basis for solving clinical problems designed to reduce the level of visual impairment due to ROP.

Purpose: the search for new molecular participants in the development of ROP to build a pathogenetically sustainable basis for improving screening, monitoring, prevention and treatment of the disease.

Material and methods: a comprehensive clinical and experimental study was carried out (763 premature infants of the risk group for ROP were examined in the clinic and 145 Wistar rat pups were included in the experiment), including an assessment of the local and systemic level of 49 cytokines of various biological effects, 4 monoamines and angiotensin-II (AT-II) at different stages of the development of the pathological process.

Results: 8 potential laboratory markers of development and unfavorable course of ROP were identified: content of MCP1 > 95 pg/ml, IGF-II > 140 pg/ml, TGF-β1 < 18000 pg/ml and IGF-I < 24 pg/mg in blood serum in premature infants before the first signs of the disease and content of VEGF-A > 108 pg/ml, TGFβ2 > 100 pg/ml, PDGF-BB > 1800 pg/ml, the serotonin < 17.0 pg/ml in blood serum in premature infants with ROP manifestation. L-DOPA and AT-II indicated its prognostic function in the experiment. All of the listed molecular agents can also be considered as targets for the development of new drugs serving for the prevention and treatment of ROP.

Conclusion: a pathogenetically substantiated basis is build for the development of new drug treatments and prevention of ROP, as well as outline ways to improve the ROP screening system.

Keywords: Retinopathy of Prematurity; Pathogenesis; Screening; Prevention; Treatment

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Citation

Citation: Osipova NA., et al. “Studying the Pathogenesis of Retinopathy of Prematurity - From Theory to Practice”.Acta Scientific Medical Sciences 5.11 (2021): 128-135.

Copyright

Copyright: © 2021 Osipova NA., et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.