<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE338nnn/GSE338573/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE338573</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>DPSCs Transfer Mitochondria via TNTs to Drive Hypoxic Angiogenesis</name><description>The dental pulp resides within a rigid dentin chamber with a limited blood supply, creating a hypoxic environment that impedes tissue regeneration. This study identifies intercellular mitochondrial transfer as a critical endogenous rescue mechanism. Human dental pulp stem cells (DPSCs) actively transfer functional mitochondria to green fluorescent protein-expressing human umbilical vein endothelial cells (GFP-ECs) under hypoxic stress. This transfer significantly reduces hypoxia-induced apoptosis, preserves mitochondrial membrane potential, and enhances the angiogenic capacities of recipient ECs. To uncover the molecular mechanisms driving this phenotype, RNA-sequencing (RNA-seq) was performed on mitochondrial-transferred ECs (Mito(+)) and control ECs (Mito(-)) under hypoxia.</description><dates><publication>2026/07/15</publication></dates><accession>GSE338573</accession><cross_references><GSM>GSM9877639</GSM><GSM>GSM9877635</GSM><GSM>GSM9877636</GSM><GSM>GSM9877637</GSM><GSM>GSM9877638</GSM><GSM>GSM9877640</GSM><GPL>24676</GPL><GSE>338573</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>