<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>35</volume><submitter>Liu X</submitter><pubmed_abstract>Choroidal neovascularization (CNV), characterized by abnormal vessel growth and vascular leakage, is the hallmark of wet age-related macular degeneration (wAMD) and a leading cause of irreversible vision loss. Although anti-vascular endothelial growth factor (VEGF) therapies remain the current standard, their frequent administration and limited long-term efficacy highlight the need for novel treatments. Here, we developed a miR-22-3p-loaded tetrahedral framework nucleic acids (tFNAs-miR22) nanostructure and evaluated its efficacy in CNV suppression. The nanocomplex was structurally validated, exhibiting high assembly fidelity and superior intraocular stability compared to serum conditions. In a laser-induced CNV mouse model, a single intravitreal injection of tFNAs-miR22 significantly redu</pubmed_abstract><journal>Materials today. Bio</journal><pagination>102578</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12719782</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Sustained suppression of choroidal neovascularization by intraocularly stable tetrahedral network encapsulated miR-22-3p.</pubmed_title><pmcid>PMC12719782</pmcid><pubmed_authors>Liu X</pubmed_authors><pubmed_authors>Cai T</pubmed_authors><pubmed_authors>Ding X</pubmed_authors><pubmed_authors>Wang Q</pubmed_authors><pubmed_authors>Li S</pubmed_authors><pubmed_authors>Huang J</pubmed_authors><pubmed_authors>Chen L</pubmed_authors><pubmed_authors>Yu G</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Luo D</pubmed_authors></additional><is_claimable>false</is_claimable><name>Sustained suppression of choroidal neovascularization by intraocularly stable tetrahedral network encapsulated miR-22-3p.</name><description>Choroidal neovascularization (CNV), characterized by abnormal vessel growth and vascular leakage, is the hallmark of wet age-related macular degeneration (wAMD) and a leading cause of irreversible vision loss. Although anti-vascular endothelial growth factor (VEGF) therapies remain the current standard, their frequent administration and limited long-term efficacy highlight the need for novel treatments. Here, we developed a miR-22-3p-loaded tetrahedral framework nucleic acids (tFNAs-miR22) nanostructure and evaluated its efficacy in CNV suppression. The nanocomplex was structurally validated, exhibiting high assembly fidelity and superior intraocular stability compared to serum conditions. In a laser-induced CNV mouse model, a single intravitreal injection of tFNAs-miR22 significantly redu</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Dec</publication><modification>2026-06-06T05:27:41.385Z</modification><creation>2026-05-26T03:12:05.497Z</creation></dates><accession>S-EPMC12719782</accession><cross_references><pubmed>41438708</pubmed><doi>10.1016/j.mtbio.2025.102578</doi></cross_references></HashMap>