| Pathological phenomenon(s) | Related signal molecule(s) | Notes | Ref. |
| Angiogenesis | HMGB-1, VEGF, sVE-cadherin, sEng | HMGB-1, VEGF, sVE-cadherin, and sEng levels were higher in PDR patients than in nondiabetics. HMGB-1 was positively correlated with sVE-cadherin. | [53] |
| Angiogenesis | HMGB-1, RAGE, VEGF, CXCL12/CXCR4, HIF-1α, early growth response-1, tyrosine kinase-2 | HMGB-1 induced upregulation of CXCL12/CXCR4, HIF-1α, early growth response-1, and tyrosine kinase-2 in diabetic retinas. HMGB-1 induced VEGF and VEGFR2 expression in HRMEC. | [54] |
| Angiogenesis and fibrosis | HMGB-1, OPN, CTGF | Upregulated HMGB-1 level in PDR and PVR patients compared with quiescent RD patients. | [55] |
| Neovascularization | HMGB-1, VEGF-A | HMGB-1 mediated AGE-induced VEGF-A production in RGC-5 cells. | [56] |
| Inflammation, neovascularization, and hemorrhage | HMGB-1, MCP-1, sICAM-1 | HMGB-1 was related to neovascularization and hemorrhage in PDR patients. HMGB-1 expression was upregulated in the retinas of diabetic mice. | [57] |
| Inflammation and disrupted retinal vascular barrier | HMGB-1, RAGE, ERK, NF-κB, ICAM-1 | Increased expression of HMGB-1, RAGE, ERK, and NF-κB in diabetic retinas. HMGB-1 reduced transendothelial electrical resistance of bovine retinal endothelial cells. HMGB-1 induced upregulation of ICAM-1, sICAM-1, HMGB-1, RAGE, ERK, and NF-κB and increased retinal vascular permeability. | [58] |
| Inflammation | HMGB-1, RAGE, NF-κB | Cytoplasmic translocation of HMGB-1 in diabetes and high glucose in retinal pericytes. | [59] |
| Inflammation | HMGB-1, NF-κB, TNF-α, VEGF | HMGB-1, receptors for HMGB-1, NF-κB, TNF-α, and VEGF were upregulated in diabetic retinas and HG-induced ARPE-19 cells. HMGB-1 blockage alleviated HG-induced expression of NF-κB and VEGF in ARPE-19 cells. | [29] |
| Apoptosis | HMGB-1, TLR4, NF-κB | Inhibition of HMGB-1 decreased expressions of TLR4 and NF-κB in high-glucose-induced RGC-5 cells. | [60] |
| Apoptosis | HMGB-1, NADPH oxidase, IL-1beta, Nox2, PARP-1, caspase-3 | HMGB-1 and oxidative stress levels in vitreous fluid from PDR patients were higher than in controls. HMGB-1 was positively associated with oxidative stress level. HMGB-1 induced IL-1beta, ROS, Nox2, PARP-1, and cleaved caspase-3 expressions in HRMEC and in the retinas of rats. | [61] |
| Apoptosis | HMGB-1, RAGE | HMGB-1/RAGE expressions as well as apoptosis cells in diabetic rat retina were higher than in controls. | [62] |
| Neurodegeneration | HMGB-1, BDNF, TBARS, caspase-3, sRAGE, sICAM-1 | Decreased serum BDNF and increased serum HMGB-1, sRAGE, sICAM-1, and TBARS in PDR patients. HMGB-1 was negatively correlated with BDNF. HMGB-1 induced upregulation of TBARS and cleaved caspase-3 and downregulated expression of BDNF and synaptophysin in rat retinas. | [63] |
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