<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/GSE322nnn/GSE322720/</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=GSE322720</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>ECM1 produced by hepatic stellate cells serves as gate keeper of liver homeostasis in hepatic fibrosis</name><description>Hepatic stellate cell (HSC) activation is central to liver fibrosis, but emerging evidence suggests HSC homeostatic activity. We compared HSC functions in parenchymal injury (CCl₄-driven) versus metabolic dysfunction-associated steatohepatitis (MASH; choline deficient high fat diet, CD-HFD) and identify therapeutic targets preserving HSC homeostatic functions.</description><dates><publication>2026/08/26</publication></dates><accession>GSE322720</accession><cross_references><GSM>GSM9557330</GSM><GSM>GSM9557310</GSM><GSM>GSM9557332</GSM><GSM>GSM9557331</GSM><GSM>GSM9557312</GSM><GSM>GSM9557311</GSM><GSM>GSM9557314</GSM><GSM>GSM9557313</GSM><GSM>GSM9557316</GSM><GSM>GSM9557315</GSM><GSM>GSM9557318</GSM><GSM>GSM9557317</GSM><GSM>GSM9557319</GSM><GSM>GSM9557321</GSM><GSM>GSM9557320</GSM><GSM>GSM9557323</GSM><GSM>GSM9557322</GSM><GSM>GSM9557325</GSM><GSM>GSM9557324</GSM><GSM>GSM9557327</GSM><GSM>GSM9557326</GSM><GSM>GSM9557329</GSM><GSM>GSM9557307</GSM><GSM>GSM9557328</GSM><GSM>GSM9557306</GSM><GSM>GSM9557309</GSM><GSM>GSM9557308</GSM><GPL>34290</GPL><GSE>322720</GSE><taxon>Mus musculus</taxon><PMID>[41854361]</PMID></cross_references></HashMap>