Full metadata record
| DC Field | Value | Language |
|---|---|---|
| dc.contributor | School of Optometry | en_US |
| dc.contributor.advisor | Do, Chi-wai (SO) | en_US |
| dc.contributor.advisor | Wen, Chunyi (BME) | en_US |
| dc.creator | Cui, Yingkun | - |
| dc.identifier.uri | https://theses.lib.polyu.edu.hk/handle/200/14451 | - |
| dc.language | English | en_US |
| dc.publisher | Hong Kong Polytechnic University | en_US |
| dc.rights | All rights reserved | en_US |
| dc.title | Systemic hypertension leads to declined retinal functions via neuroinflammation-related pathways | en_US |
| dcterms.abstract | Systemic hypertension (HT) is a leading cause of premature death globally. Glaucoma, a common eye disease, is the major cause of irreversible blindness worldwide. Despite their prevalence, the relationship between HT and glaucoma risk remains elusive. The interaction between blood pressure (BP) and intraocular pressure (IOP), a major glaucoma risk factor, is not fully understood. This study investigated the effects of chronic HT on IOP, retinal function, and structure across different HT stages, employing transcriptomic analysis to explore molecular retinal changes. We also studied the impact of endothelin-2 (EDN2) knockout and endothelin receptor antagonists on IOP and retinal function. | en_US |
| dcterms.abstract | Using spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) as models, we measured BP, IOP, retinal function, structure, and vessel lumen areas at 4, 8, and 12 months, both cross-sectionally and longitudinally. SHR exhibited consistently higher BP but surprisingly lower IOP than WKY. Retinal functional responses were similar at 4 months but significantly reduced in SHR at 8 and 12 months compared to WKY. SHR displayed thinner total retinal and inner plexiform layers from 4 months onward. Both retinal arteries and veins had markedly narrower lumens in SHR at all time points, suggesting reduced retinal blood flow. | en_US |
| dcterms.abstract | Transcriptomic analysis of SHR retinas at 8 months revealed upregulation of inflammatory pathways, including leukocyte migration, chemokine signaling, complement and coagulation cascades, and cytokine-receptor interactions. By 12 months, neuroinflammation-related pathways such as Toll-like receptor and NF-κB signaling were also upregulated. SHR showed fewer retinal ganglion cells at 8 and 12 months and enlarged, more numerous microglia at 12 months. Elevated EDN2 expression was found in 8-month SHR retinas at both mRNA and protein levels. These findings strongly suggest that retinal degeneration in SHR is primarily driven by mechanisms independent of IOP and increased neuroinflammation. | en_US |
| dcterms.abstract | To confirm the involvement of the endothelin system, adeno-associated virus-mediated EDN2 knockout and intravitreal injections of endothelin receptor antagonists (Bq123 for EDNRA and Bq788 for EDNRB) were performed. EDN2 knockout enhanced retinal function in SHR without influencing IOP and suppressed inflammatory pathways. Similarly, Bq123 lowered IOP in WKY but not SHR, but improved SHR retinal function and downregulated retinal mRNA of IL-1α, endothelin-1, and EDNRA. Bq788 showed no significant effects. These results indicate the involvement of EDN2 and EDNRA in HT-induced retinal degeneration, and targeting these pathways may alleviate retinal damage. | en_US |
| dcterms.abstract | In summary, we demonstrate that chronic HT contributes to retinal degeneration primarily through impaired blood flow and inflammation rather than elevated IOP, with endothelin signaling playing a significant role. Our results provide new insights into therapeutic strategies for treating HT-related retinal diseases. | en_US |
| dcterms.extent | 174 pages : color illustrations | en_US |
| dcterms.isPartOf | PolyU Electronic Theses | en_US |
| dcterms.issued | 2026 | en_US |
| dcterms.educationalLevel | Ph.D. | en_US |
| dcterms.educationalLevel | All Doctorate | en_US |
| dcterms.LCSH | Hypertension | en_US |
| dcterms.LCSH | Intraocular pressure | en_US |
| dcterms.LCSH | Retina -- Diseases | en_US |
| dcterms.LCSH | Hong Kong Polytechnic University -- Dissertations | en_US |
| dcterms.accessRights | open access | en_US |
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