2023
DOI: 10.1089/wound.2021.0102
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Multifunctional Elastin-Like Polypeptide Fusion Protein Coacervates Inhibit Receptor-Mediated Proinflammatory Signals and Promote Angiogenesis in Mouse Diabetic Wounds

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Cited by 7 publications
(4 citation statements)
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“…1 d) showed the top 12 signalling pathways, many of which were closely associated with a variety of chronic wounds, such as apoptosis 70 , HIF-1 signalling pathways 71 and ROS 72 . Additionally, the AGE-RAGE signalling pathway in diabetic complications 73 was involved in diabetic wound healing; hepatitis B 74 , human cytomegalovirus infection and hepatitis C 75 signalling pathways might participate in chronic infectious wounds 76 . As shown in Fig.…”
Section: Resultsmentioning
confidence: 99%
“…1 d) showed the top 12 signalling pathways, many of which were closely associated with a variety of chronic wounds, such as apoptosis 70 , HIF-1 signalling pathways 71 and ROS 72 . Additionally, the AGE-RAGE signalling pathway in diabetic complications 73 was involved in diabetic wound healing; hepatitis B 74 , human cytomegalovirus infection and hepatitis C 75 signalling pathways might participate in chronic infectious wounds 76 . As shown in Fig.…”
Section: Resultsmentioning
confidence: 99%
“…Furthermore, several studies have con rmed conclusively the role of AGEs-RAGE in DFU development [29,30]. Hyperglycemia made induction of non-enzymatic glycosylation of proteins and lipids for AGEs formation, which, following binding to their receptor RAGE, further causing pro-in ammatory signaling and vascular endothelial damage, thereby delaying diabetic wound healing [30]. The application of ibrutinib by Yang et al [29] [29] revealed that it led to lower RAGE, IL-1β, TNF-α, and IL-6 expression, whereas upregulated VEGF levels, which caused higher wound healing rate and wound healing promotion of DFU rats, matching ndings of the present study.…”
Section: Discussionmentioning
confidence: 99%
“…Li et al [25] [25] demonstrated that hesperidin treatment resulted in an increase in SOD and GSH levels, whereas a decrease in MDA and NO levels, while reversing down-regulation of VEGF-c, Ang-1, and Tie-2 expression occurred in wound tissues of DFU rats, in high accordance with our study. Furthermore, several studies have con rmed conclusively the role of AGEs-RAGE in DFU development [29,30]. Hyperglycemia made induction of non-enzymatic glycosylation of proteins and lipids for AGEs formation, which, following binding to their receptor RAGE, further causing pro-in ammatory signaling and vascular endothelial damage, thereby delaying diabetic wound healing [30].…”
Section: Discussionmentioning
confidence: 99%
“…Encouragingly, an anti-RAGE monoclonal antibody that binds a peptide sequence in the RAGE extracellular structural domain prevented receptor-ligand binding and significantly improved hindlimb perfusion in ischaemic limbs, with greater reconstruction of collateral circulation in occluded arteries [ 132 ]. Recombinant proteins containing ELP fused to the RAGE domain or to stromal cell-derived factor 1 can inhibit AGE-RAGE signal transduction and promote cell proliferation and angiogenesis [ 133 ]. Blocking the AGE-RAGE-based response involving matrix proteins is emerging as a promising approach for preventing the development of ischaemic diseases in older adults.…”
Section: Therapeutic Strategies For Promoting Angiogenesis By Targeti...mentioning
confidence: 99%