PMC:7572937 / 35787-36801 JSONTXT

{"project":"MyTest","denotations":[{"id":"33082511-29643724-29997645","span":{"begin":659,"end":663},"obj":"29643724"},{"id":"33082511-16723446-29997646","span":{"begin":814,"end":816},"obj":"16723446"},{"id":"33082511-24790856-29997647","span":{"begin":943,"end":946},"obj":"24790856"}],"namespaces":[{"prefix":"_base","uri":"https://www.uniprot.org/uniprot/testbase"},{"prefix":"UniProtKB","uri":"https://www.uniprot.org/uniprot/"},{"prefix":"uniprot","uri":"https://www.uniprot.org/uniprotkb/"}],"text":"Diabetes is a representative metabolic disease with ocular complications. Diabetic patients show impaired corneal wound healing because of corneal epithelium and nerve defects. RvD1 can improve corneal epithelial regeneration in diabetic mice. RvD1 acts via the following mechanisms: increased expression of proliferation-related molecules (Ki67 and SIRT1), EGFR activation, decreased inflammatory cytokine (TNF-α, IL-1β) production, decreased expression of ROS-generating enzymes (NOX2 and NOX3), and upregulated expression of antioxidant genes (Nrf2, MnSOD, and HO-1). WRW4, the FPR2 antagonist, significantly blocks these various therapeutic effects of RvD1106. Another FPR2 ligand, LL-37, also promotes corneal epithelial cell migration in a PTX- and FPR2-sensitive manner and facilitates corneal wound healing95. Regarding SAA, the expression of Saa1,3 was increased with the expression of Fpr2 in a corneal neovascularization mouse model102. This pattern implies that SAA-FPR2 plays a role in this condition."}

{"project":"2_test","denotations":[{"id":"33082511-29643724-29997645","span":{"begin":659,"end":663},"obj":"29643724"},{"id":"33082511-16723446-29997646","span":{"begin":814,"end":816},"obj":"16723446"},{"id":"33082511-24790856-29997647","span":{"begin":943,"end":946},"obj":"24790856"}],"text":"Diabetes is a representative metabolic disease with ocular complications. Diabetic patients show impaired corneal wound healing because of corneal epithelium and nerve defects. RvD1 can improve corneal epithelial regeneration in diabetic mice. RvD1 acts via the following mechanisms: increased expression of proliferation-related molecules (Ki67 and SIRT1), EGFR activation, decreased inflammatory cytokine (TNF-α, IL-1β) production, decreased expression of ROS-generating enzymes (NOX2 and NOX3), and upregulated expression of antioxidant genes (Nrf2, MnSOD, and HO-1). WRW4, the FPR2 antagonist, significantly blocks these various therapeutic effects of RvD1106. Another FPR2 ligand, LL-37, also promotes corneal epithelial cell migration in a PTX- and FPR2-sensitive manner and facilitates corneal wound healing95. Regarding SAA, the expression of Saa1,3 was increased with the expression of Fpr2 in a corneal neovascularization mouse model102. This pattern implies that SAA-FPR2 plays a role in this condition."}