<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Garvin AM</submitter><funding>BLRD VA</funding><funding>NHLBI NIH HHS</funding><pagination>904-918</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7878436</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>77(3)</volume><pubmed_abstract>Transient ACE (angiotensin-converting enzyme) inhibition in spontaneously hypertensive rats is known to protect against future injury-induced cardiac inflammation, fibrosis, and dysfunction; however, the mechanisms of protection have not been delineated. Here, we used single-cell RNA sequencing to test the hypothesis that transient ACE inhibitor treatment would induce a persistent shift in cardiac fibroblast subpopulations. Adult male spontaneously hypertensive rats (11 weeks old, hypertensive with cardiac hypertrophy) were treated for 2 weeks with an ACE inhibitor, enalapril (30 mg/kg per day, PO), or water (untreated spontaneously hypertensive rats) followed by a 2-week washout period (n=7/group). Cardiac fibroblasts were isolated from the left ventricle and subjected to single-cell RNA </pubmed_abstract><journal>Hypertension (Dallas, Tex. : 1979)</journal><pubmed_title>Transient ACE (Angiotensin-Converting Enzyme) Inhibition Suppresses Future Fibrogenic Capacity and Heterogeneity of Cardiac Fibroblast Subpopulations.</pubmed_title><pmcid>PMC7878436</pmcid><funding_grant_id>R56 HL141165</funding_grant_id><funding_grant_id>I01 BX000505</funding_grant_id><funding_grant_id>R01 HL137319</funding_grant_id><funding_grant_id>R01 HL129823</funding_grant_id><pubmed_authors>Garvin AM</pubmed_authors><pubmed_authors>Hale TM</pubmed_authors><pubmed_authors>De Both MD</pubmed_authors><pubmed_authors>Lindsey ML</pubmed_authors><pubmed_authors>Talboom JS</pubmed_authors><pubmed_authors>Huentelman MJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Transient ACE (Angiotensin-Converting Enzyme) Inhibition Suppresses Future Fibrogenic Capacity and Heterogeneity of Cardiac Fibroblast Subpopulations.</name><description>Transient ACE (angiotensin-converting enzyme) inhibition in spontaneously hypertensive rats is known to protect against future injury-induced cardiac inflammation, fibrosis, and dysfunction; however, the mechanisms of protection have not been delineated. Here, we used single-cell RNA sequencing to test the hypothesis that transient ACE inhibitor treatment would induce a persistent shift in cardiac fibroblast subpopulations. Adult male spontaneously hypertensive rats (11 weeks old, hypertensive with cardiac hypertrophy) were treated for 2 weeks with an ACE inhibitor, enalapril (30 mg/kg per day, PO), or water (untreated spontaneously hypertensive rats) followed by a 2-week washout period (n=7/group). Cardiac fibroblasts were isolated from the left ventricle and subjected to single-cell RNA </description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Mar</publication><modification>2026-05-02T11:23:18.791Z</modification><creation>2025-02-19T03:26:26.997Z</creation></dates><accession>S-EPMC7878436</accession><cross_references><pubmed>33486989</pubmed><doi>10.1161/HYPERTENSIONAHA.120.16352</doi><doi>10.1161/hypertensionaha.120.16352</doi></cross_references></HashMap>