<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/GSE330nnn/GSE330352/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</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=GSE330352</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Panax notoginseng -derived extracellular vesicles alleviate doxorubicin-induced cardiotoxicity by suppressing p53 activation</name><description>Doxorubicin (Dox) is a highly effective chemotherapeutic agent, but its clinical use is limited by cumulative cardiotoxicity. Panax notoginseng, a traditional medicinal herb, exhibits well-documented cardioprotective properties; however, the therapeutic application of its bioactive constituents is constrained by poor bioavailability and potential toxicity. Plant-derived extracellular vesicles (EVs) have emerged as natural nanocarriers facilitating cross-kingdom delivery of bioactive metabolites. In this study, we investigated whether P. notoginseng-derived EVs (PEVs) could mitigate Dox-induced cardiotoxicity (DIC) and explored the underlying mechanisms.</description><dates><publication>2026/05/08</publication></dates><accession>GSE330352</accession><cross_references><GSM>GSM9724309</GSM><GSM>GSM9724308</GSM><GSM>GSM9724307</GSM><GSM>GSM9724315</GSM><GSM>GSM9724314</GSM><GSM>GSM9724313</GSM><GSM>GSM9724312</GSM><GSM>GSM9724311</GSM><GSM>GSM9724310</GSM><GPL>34290</GPL><GSE>330352</GSE><taxon>Mus musculus</taxon><PMID>[42090956]</PMID></cross_references></HashMap>