<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Shao X</submitter><funding>National Natural Science Foundation of China</funding><pagination>e1344</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10366349</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(7)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>The first-line therapy is effective for the treatment of primary immune thrombocytopenia (ITP); however, maintaining the long-term responses remains challenging. Low-dose decitabine (DAC) has been adopted to treat refractory ITP, while its role in macrophage polarization has not been fully understood. We aimed to investigate the mechanistic role of DAC in M2 macrophage polarization and evaluated its therapeutic effect in ITP.&lt;h4>Methods&lt;/h4>The M2 monocytes were identified by flow cytometry from peripheral blood mononuclear cells in healthy controls (HCs) and ITP patients. The expression of PPARγ, Arg-1, DNMT3b and NLRP3, together with IL-10 plasma levels was measured to examine its function. Bisulfite-sequencing PCR was used to evaluate the methylation status of PPARγ p</pubmed_abstract><journal>Clinical and translational medicine</journal><pubmed_title>Low-dose decitabine promotes M2 macrophage polarization in patients with primary immune thrombocytopenia via enhancing KLF4 binding to PPARγ promoter.</pubmed_title><pmcid>PMC10366349</pmcid><funding_grant_id>81870098</funding_grant_id><funding_grant_id>82200135</funding_grant_id><pubmed_authors>Xu P</pubmed_authors><pubmed_authors>Li F</pubmed_authors><pubmed_authors>Ji L</pubmed_authors><pubmed_authors>Zhuang X</pubmed_authors><pubmed_authors>Wu B</pubmed_authors><pubmed_authors>Chen H</pubmed_authors><pubmed_authors>Cheng Y</pubmed_authors><pubmed_authors>Zhan Y</pubmed_authors><pubmed_authors>Sun L</pubmed_authors><pubmed_authors>Shao X</pubmed_authors><pubmed_authors>Hua F</pubmed_authors><pubmed_authors>Ou Y</pubmed_authors><pubmed_authors>Wang X</pubmed_authors></additional><is_claimable>false</is_claimable><name>Low-dose decitabine promotes M2 macrophage polarization in patients with primary immune thrombocytopenia via enhancing KLF4 binding to PPARγ promoter.</name><description>&lt;h4>Background&lt;/h4>The first-line therapy is effective for the treatment of primary immune thrombocytopenia (ITP); however, maintaining the long-term responses remains challenging. Low-dose decitabine (DAC) has been adopted to treat refractory ITP, while its role in macrophage polarization has not been fully understood. We aimed to investigate the mechanistic role of DAC in M2 macrophage polarization and evaluated its therapeutic effect in ITP.&lt;h4>Methods&lt;/h4>The M2 monocytes were identified by flow cytometry from peripheral blood mononuclear cells in healthy controls (HCs) and ITP patients. The expression of PPARγ, Arg-1, DNMT3b and NLRP3, together with IL-10 plasma levels was measured to examine its function. Bisulfite-sequencing PCR was used to evaluate the methylation status of PPARγ p</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jul</publication><modification>2025-04-22T13:35:24.665Z</modification><creation>2025-04-22T13:35:24.665Z</creation></dates><accession>S-EPMC10366349</accession><cross_references><pubmed>37488670</pubmed><doi>10.1002/ctm2.1344</doi></cross_references></HashMap>