<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Morningstar JE</submitter><funding>NCATS NIH HHS</funding><funding>NCRR NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>e022332</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9075228</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(24)</volume><pubmed_abstract>Background Mitral valve prolapse (MVP) is one of the most common forms of cardiac valve disease and affects 2% to 3% of the population. Previous imaging reports have indicated that myocardial fibrosis is common in MVP and described its association with sudden cardiac death. These data combined with evidence for postrepair ventricular dysfunction in surgical patients with MVP support a link between fibrosis and MVP. Methods and Results We performed histopathologic analysis of left ventricular (LV) biopsies from peripapillary regions, inferobasal LV wall and apex on surgical patients with MVP, as well as in a mouse model of human MVP (&lt;i>Dzip1&lt;sup>S14R&lt;/sup>&lt;/i>&lt;i>&lt;sup>/+&lt;/sup>&lt;/i>). Tension-dependent molecular pathways were subsequently assessed using both computational modeling and cyclica</pubmed_abstract><journal>Journal of the American Heart Association</journal><pubmed_title>Mitral Valve Prolapse Induces Regionalized Myocardial Fibrosis.</pubmed_title><pmcid>PMC9075228</pmcid><funding_grant_id>UL1 TR001450</funding_grant_id><funding_grant_id>T32 HL007260</funding_grant_id><funding_grant_id>T32 GM132055</funding_grant_id><funding_grant_id>P20 GM103444</funding_grant_id><funding_grant_id>R01 HL149696</funding_grant_id><funding_grant_id>F31 HL142159</funding_grant_id><funding_grant_id>C06 RR018823</funding_grant_id><funding_grant_id>F31 HL152494</funding_grant_id><funding_grant_id>R35 HL161237</funding_grant_id><funding_grant_id>R25 GM113278</funding_grant_id><funding_grant_id>R01 HL131546</funding_grant_id><funding_grant_id>R01 HL141855</funding_grant_id><pubmed_authors>Bertrand P</pubmed_authors><pubmed_authors>Poelzing S</pubmed_authors><pubmed_authors>Norris RA</pubmed_authors><pubmed_authors>Wang C</pubmed_authors><pubmed_authors>Fulmer D</pubmed_authors><pubmed_authors>Sieg F</pubmed_authors><pubmed_authors>Moore R</pubmed_authors><pubmed_authors>Watts K</pubmed_authors><pubmed_authors>Spampinato RA</pubmed_authors><pubmed_authors>Gensemer C</pubmed_authors><pubmed_authors>Glover J</pubmed_authors><pubmed_authors>Gourdie RG</pubmed_authors><pubmed_authors>Moore K</pubmed_authors><pubmed_authors>Borger MA</pubmed_authors><pubmed_authors>Guo L</pubmed_authors><pubmed_authors>Richardson WJ</pubmed_authors><pubmed_authors>Morningstar JE</pubmed_authors><pubmed_authors>Nagata Y</pubmed_authors><pubmed_authors>Beck TC</pubmed_authors><pubmed_authors>Levine RA</pubmed_authors></additional><is_claimable>false</is_claimable><name>Mitral Valve Prolapse Induces Regionalized Myocardial Fibrosis.</name><description>Background Mitral valve prolapse (MVP) is one of the most common forms of cardiac valve disease and affects 2% to 3% of the population. Previous imaging reports have indicated that myocardial fibrosis is common in MVP and described its association with sudden cardiac death. These data combined with evidence for postrepair ventricular dysfunction in surgical patients with MVP support a link between fibrosis and MVP. Methods and Results We performed histopathologic analysis of left ventricular (LV) biopsies from peripapillary regions, inferobasal LV wall and apex on surgical patients with MVP, as well as in a mouse model of human MVP (&lt;i>Dzip1&lt;sup>S14R&lt;/sup>&lt;/i>&lt;i>&lt;sup>/+&lt;/sup>&lt;/i>). Tension-dependent molecular pathways were subsequently assessed using both computational modeling and cyclica</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Dec</publication><modification>2026-06-04T04:38:36.759Z</modification><creation>2025-04-04T07:47:07.232Z</creation></dates><accession>S-EPMC9075228</accession><cross_references><pubmed>34873924</pubmed><doi>10.1161/JAHA.121.022332</doi></cross_references></HashMap>