<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Li X</submitter><funding>the Foundation of National Infrastructures for Translational Medicine (Shanghai)</funding><funding>the Foundation of National Infrastructures for Translational Medicine</funding><funding>the National Natural Science Foundation of China</funding><funding>Innovative research team of high-level local universities in Shanghai</funding><pagination>249</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11241881</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>23(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Previous studies have shown that peptides encoded by noncoding RNAs (ncRNAs) can be used as peptide drugs to alleviate diseases. We found that microRNA-31 (miR-31) is involved in the regulation of hypertension and that the peptide miPEP31, which is encoded by the primary transcript of miR-31 (pri-miR-31), can inhibit miR-31 expression. However, the role and mechanism of miPEP31 in hypertension have not been elucidated.&lt;h4>Methods&lt;/h4>miPEP31 expression was determined by western blot analysis. miPEP31-deficient mice (miPEP31&lt;sup>-/-&lt;/sup>) were used, and synthetic miPEP31 was injected into Ang II-induced hypertensive mice. Blood pressure was monitored through the tail-cuff method. Histological staining was used to evaluate renal damage. Regulatory T (T&lt;sub>reg&lt;/sub>) cell</pubmed_abstract><journal>Cardiovascular diabetology</journal><pubmed_title>miPEP31 alleviates Ang II-induced hypertension in mice by occupying Cebpα binding sites in the pri-miR-31 promoter.</pubmed_title><pmcid>PMC11241881</pmcid><funding_grant_id>82070509</funding_grant_id><funding_grant_id>SHSMU-ZDCX20212700</funding_grant_id><funding_grant_id>82370902</funding_grant_id><funding_grant_id>82101909</funding_grant_id><funding_grant_id>TMSK-2021-506</funding_grant_id><pubmed_authors>Tian J</pubmed_authors><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Fang Z</pubmed_authors><pubmed_authors>Jiang G</pubmed_authors><pubmed_authors>Chen W</pubmed_authors><pubmed_authors>Shi G</pubmed_authors><pubmed_authors>Tong X</pubmed_authors><pubmed_authors>Li Q</pubmed_authors><pubmed_authors>Zhou H</pubmed_authors><pubmed_authors>Lu P</pubmed_authors><pubmed_authors>Zhang P</pubmed_authors></additional><is_claimable>false</is_claimable><name>miPEP31 alleviates Ang II-induced hypertension in mice by occupying Cebpα binding sites in the pri-miR-31 promoter.</name><description>&lt;h4>Background&lt;/h4>Previous studies have shown that peptides encoded by noncoding RNAs (ncRNAs) can be used as peptide drugs to alleviate diseases. We found that microRNA-31 (miR-31) is involved in the regulation of hypertension and that the peptide miPEP31, which is encoded by the primary transcript of miR-31 (pri-miR-31), can inhibit miR-31 expression. However, the role and mechanism of miPEP31 in hypertension have not been elucidated.&lt;h4>Methods&lt;/h4>miPEP31 expression was determined by western blot analysis. miPEP31-deficient mice (miPEP31&lt;sup>-/-&lt;/sup>) were used, and synthetic miPEP31 was injected into Ang II-induced hypertensive mice. Blood pressure was monitored through the tail-cuff method. Histological staining was used to evaluate renal damage. Regulatory T (T&lt;sub>reg&lt;/sub>) cell</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jul</publication><modification>2025-04-27T01:01:44.356Z</modification><creation>2025-04-06T18:03:56.207Z</creation></dates><accession>S-EPMC11241881</accession><cross_references><pubmed>38992718</pubmed><doi>10.1186/s12933-024-02337-5</doi></cross_references></HashMap>