<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Pedersen LN</submitter><funding>NIBIB NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>NIAID NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>NCI NIH HHS</funding><funding>NIH HHS</funding><pagination>928-943.e5</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10994563</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>4(12)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Rapidly dividing cells are more sensitive to radiation therapy (RT) than quiescent cells. In the failing myocardium, macrophages and fibroblasts mediate collateral tissue injury, leading to progressive myocardial remodeling, fibrosis, and pump failure. Because these cells divide more rapidly than cardiomyocytes, we hypothesized that macrophages and fibroblasts would be more susceptible to lower doses of radiation and that cardiac radiation could therefore attenuate myocardial remodeling.&lt;h4>Methods&lt;/h4>In three independent murine heart failure models, including models of metabolic stress, ischemia, and pressure overload, mice underwent 5 Gy cardiac radiation or sham treatment followed by echocardiography. Immunofluorescence, flow cytometry, and non-invasive PET imaging w</pubmed_abstract><journal>Med (New York, N.Y.)</journal><pubmed_title>Cardiac radiation improves ventricular function in mice and humans with cardiomyopathy.</pubmed_title><pmcid>PMC10994563</pmcid><funding_grant_id>T32 CA113275</funding_grant_id><funding_grant_id>R35 HL161185</funding_grant_id><funding_grant_id>R01 HL155344</funding_grant_id><funding_grant_id>K08 HL138262</funding_grant_id><funding_grant_id>S10 OD030403</funding_grant_id><funding_grant_id>P30 DK020579</funding_grant_id><funding_grant_id>R35 HL145212</funding_grant_id><funding_grant_id>P30 DK052574</funding_grant_id><funding_grant_id>P30 DK056341</funding_grant_id><funding_grant_id>P30 CA091842</funding_grant_id><funding_grant_id>R01 HL163274</funding_grant_id><funding_grant_id>T32 AI007163</funding_grant_id><funding_grant_id>R01 HL147884</funding_grant_id><funding_grant_id>T32 HL007081</funding_grant_id><funding_grant_id>S10 OD028597</funding_grant_id><funding_grant_id>P41 EB025815</funding_grant_id><funding_grant_id>S10 OD020136</funding_grant_id><pubmed_authors>Cuculich PS</pubmed_authors><pubmed_authors>Hugo G</pubmed_authors><pubmed_authors>Guo Z</pubmed_authors><pubmed_authors>Lavine K</pubmed_authors><pubmed_authors>Weinheimer C</pubmed_authors><pubmed_authors>Grogan F</pubmed_authors><pubmed_authors>Zhang S</pubmed_authors><pubmed_authors>Ozcan M</pubmed_authors><pubmed_authors>Strong L</pubmed_authors><pubmed_authors>Klaas A</pubmed_authors><pubmed_authors>Liu Y</pubmed_authors><pubmed_authors>Bergom C</pubmed_authors><pubmed_authors>Woodard PK</pubmed_authors><pubmed_authors>Diab A</pubmed_authors><pubmed_authors>Rentschler SL</pubmed_authors><pubmed_authors>Schwarz JK</pubmed_authors><pubmed_authors>Navara R</pubmed_authors><pubmed_authors>Nigro J</pubmed_authors><pubmed_authors>Valenzuela Ripoll C</pubmed_authors><pubmed_authors>Cho Y</pubmed_authors><pubmed_authors>Samson P</pubmed_authors><pubmed_authors>Ng S</pubmed_authors><pubmed_authors>Walls GM</pubmed_authors><pubmed_authors>Pedersen LN</pubmed_authors><pubmed_authors>Ataran A</pubmed_authors><pubmed_authors>Lotfinaghsh A</pubmed_authors><pubmed_authors>Kovacs A</pubmed_authors><pubmed_authors>Kolb K</pubmed_authors><pubmed_authors>Moore K</pubmed_authors><pubmed_authors>Reynoso FJ</pubmed_authors><pubmed_authors>Luehmann H</pubmed_authors><pubmed_authors>Cooper D</pubmed_authors><pubmed_authors>Robinson C</pubmed_authors><pubmed_authors>Javaheri A</pubmed_authors><pubmed_authors>Heck A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Cardiac radiation improves ventricular function in mice and humans with cardiomyopathy.</name><description>&lt;h4>Background&lt;/h4>Rapidly dividing cells are more sensitive to radiation therapy (RT) than quiescent cells. In the failing myocardium, macrophages and fibroblasts mediate collateral tissue injury, leading to progressive myocardial remodeling, fibrosis, and pump failure. Because these cells divide more rapidly than cardiomyocytes, we hypothesized that macrophages and fibroblasts would be more susceptible to lower doses of radiation and that cardiac radiation could therefore attenuate myocardial remodeling.&lt;h4>Methods&lt;/h4>In three independent murine heart failure models, including models of metabolic stress, ischemia, and pressure overload, mice underwent 5 Gy cardiac radiation or sham treatment followed by echocardiography. Immunofluorescence, flow cytometry, and non-invasive PET imaging w</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Dec</publication><modification>2026-06-02T10:48:33.026Z</modification><creation>2025-04-04T01:24:35.822Z</creation></dates><accession>S-EPMC10994563</accession><cross_references><pubmed>38029754</pubmed><doi>10.1016/j.medj.2023.10.006</doi></cross_references></HashMap>