<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yan Z</submitter><funding>American Heart Association</funding><funding>National Institutes of Health</funding><pagination>779</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8909652</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11(5)</volume><pubmed_abstract>Background The impairment of the inner blood-retinal barrier (iBRB) increases the pathological development of diabetic retinopathy (DR), a severe complication in diabetic patients. Identifying approaches to preserving iBRB integrity and function is a significant challenge in DR. C1q/tumor necrosis factor-related protein-3 (CTRP3) is a newly discovered adipokine and a vital biomarker, predicting DR severity. We sought to determine whether and how CTRP3 affects the pathological development of non-proliferative diabetic retinopathy (NPDR). Methods To clarify the pathophysiologic progress of the blood-retinal barrier in NPDR and explore its potential mechanism, a mouse Type 2 diabetic model of diabetic retinopathy was used. The capillary leakage was assessed by confocal microscope with fluores</pubmed_abstract><journal>Cells</journal><pubmed_title>C1q/TNF-Related Protein 3 Prevents Diabetic Retinopathy via AMPK-Dependent Stabilization of Blood-Retinal Barrier Tight Junctions.</pubmed_title><pmcid>PMC8909652</pmcid><funding_grant_id>TPA</funding_grant_id><funding_grant_id>96686</funding_grant_id><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Naik UP</pubmed_authors><pubmed_authors>Wang C</pubmed_authors><pubmed_authors>Ma X</pubmed_authors><pubmed_authors>Meng Z</pubmed_authors><pubmed_authors>Guo R</pubmed_authors><pubmed_authors>Xie D</pubmed_authors><pubmed_authors>Christopher TA</pubmed_authors><pubmed_authors>Yan Z</pubmed_authors><pubmed_authors>Gan L</pubmed_authors><pubmed_authors>Bond Lau W</pubmed_authors><pubmed_authors>Lopez BL</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Zhao J</pubmed_authors></additional><is_claimable>false</is_claimable><name>C1q/TNF-Related Protein 3 Prevents Diabetic Retinopathy via AMPK-Dependent Stabilization of Blood-Retinal Barrier Tight Junctions.</name><description>Background The impairment of the inner blood-retinal barrier (iBRB) increases the pathological development of diabetic retinopathy (DR), a severe complication in diabetic patients. Identifying approaches to preserving iBRB integrity and function is a significant challenge in DR. C1q/tumor necrosis factor-related protein-3 (CTRP3) is a newly discovered adipokine and a vital biomarker, predicting DR severity. We sought to determine whether and how CTRP3 affects the pathological development of non-proliferative diabetic retinopathy (NPDR). Methods To clarify the pathophysiologic progress of the blood-retinal barrier in NPDR and explore its potential mechanism, a mouse Type 2 diabetic model of diabetic retinopathy was used. The capillary leakage was assessed by confocal microscope with fluores</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Feb</publication><modification>2025-05-18T12:07:35.511Z</modification><creation>2025-05-18T12:07:35.511Z</creation></dates><accession>S-EPMC8909652</accession><cross_references><pubmed>35269401</pubmed><doi>10.3390/cells11050779</doi></cross_references></HashMap>