<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Luo L</submitter><funding>American Heart Association</funding><funding>NHLBI NIH HHS</funding><funding>National Institute of Health</funding><pagination>2703-2717</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9890476</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>118(12)</volume><pubmed_abstract>&lt;h4>Aims&lt;/h4>Intimal hyperplasia is a common feature of vascular remodelling disorders. Accumulation of synthetic smooth muscle cell (SMC)-like cells is the main underlying cause. Current therapeutic approaches including drug-eluting stents are not perfect due to the toxicity on endothelial cells and novel therapeutic strategies are needed. Our preliminary screening for dysregulated cyclic nucleotide phosphodiesterases (PDEs) in growing SMCs revealed the alteration of PDE10A expression. Herein, we investigated the function of PDE10A in SMC proliferation and intimal hyperplasia both in vitro and in vivo.&lt;h4>Methods and results&lt;/h4>RT-qPCR, immunoblot, and in situ proximity ligation assay were performed to determine PDE10A expression in synthetic SMCs and injured vessels. We found that PDE10</pubmed_abstract><journal>Cardiovascular research</journal><pubmed_title>Role of PDE10A in vascular smooth muscle cell hyperplasia and pathological vascular remodelling.</pubmed_title><pmcid>PMC9890476</pmcid><funding_grant_id>R01 HL134910</funding_grant_id><funding_grant_id>18PRE34030228</funding_grant_id><funding_grant_id>R01 HL139794</funding_grant_id><funding_grant_id>R01 HL154318</funding_grant_id><funding_grant_id>R01 HL122686</funding_grant_id><funding_grant_id>R01HL134910</funding_grant_id><funding_grant_id>R01HL154318</funding_grant_id><pubmed_authors>Long X</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Luo L</pubmed_authors><pubmed_authors>Cai Y</pubmed_authors><pubmed_authors>Korshunov VA</pubmed_authors><pubmed_authors>Berk BC</pubmed_authors><pubmed_authors>Knight PA</pubmed_authors><pubmed_authors>Yan C</pubmed_authors><pubmed_authors>Hsu CG</pubmed_authors></additional><is_claimable>false</is_claimable><name>Role of PDE10A in vascular smooth muscle cell hyperplasia and pathological vascular remodelling.</name><description>&lt;h4>Aims&lt;/h4>Intimal hyperplasia is a common feature of vascular remodelling disorders. Accumulation of synthetic smooth muscle cell (SMC)-like cells is the main underlying cause. Current therapeutic approaches including drug-eluting stents are not perfect due to the toxicity on endothelial cells and novel therapeutic strategies are needed. Our preliminary screening for dysregulated cyclic nucleotide phosphodiesterases (PDEs) in growing SMCs revealed the alteration of PDE10A expression. Herein, we investigated the function of PDE10A in SMC proliferation and intimal hyperplasia both in vitro and in vivo.&lt;h4>Methods and results&lt;/h4>RT-qPCR, immunoblot, and in situ proximity ligation assay were performed to determine PDE10A expression in synthetic SMCs and injured vessels. We found that PDE10</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Sep</publication><modification>2026-06-01T03:16:59.401Z</modification><creation>2025-02-18T23:37:24.126Z</creation></dates><accession>S-EPMC9890476</accession><cross_references><pubmed>34550322</pubmed><doi>10.1093/cvr/cvab304</doi></cross_references></HashMap>