<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>13</volume><submitter>Huang M</submitter><pubmed_abstract>Transverse aortic constriction (TAC) is a frequently used model to investigate pressure overload-induced progressive heart failure (HF); however, there is considerable phenotypic variation among different mouse strains and even sub-strains. Moreover, less is known about the TAC model in ICR mice. Therefore, to determine the suitability of the ICR strain for TAC-induced HF research, we compared the effects of TAC on ICR and C57BL/6J mice at one, two and four weeks post-TAC &lt;i>via&lt;/i> echocardiography, organ index, morphology, and histology. At the end of the study, behavior and gene expression patterns were assessed, and overall survival was monitored. Compared to the sham-operated mice, ICR and C57BL/6J mice displayed hypertrophic phenotypes with a significant increase in ventricle wall thickness, heart weight and ratio, and cross-sectional area of cardiomyocytes after a 2-week TAC exposure. In addition, ICR mice developed reduced systolic function and severe lung congestion 4 weeks post-TAC, whereas C57BL/6J did not. Besides, ICR mice demonstrated comparable survival, similar gene expression alteration but severer fibrotic remodeling and poor behavioral performance compared to the C57BL/6J mice. Our data demonstrated that ICR was quite sensitive to TAC-induced heart failure and can be an ideal research tool to investigate mechanisms and drug intervention for pressure overload-induced HF.</pubmed_abstract><journal>Frontiers in physiology</journal><pagination>1026884</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9745147</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Evaluation of the transverse aortic constriction model in ICR and C57BL/6J mice.</pubmed_title><pmcid>PMC9745147</pmcid><pubmed_authors>Wang M</pubmed_authors><pubmed_authors>Li W</pubmed_authors><pubmed_authors>Tang J</pubmed_authors><pubmed_authors>Lu L</pubmed_authors><pubmed_authors>Yu L</pubmed_authors><pubmed_authors>Ling G</pubmed_authors><pubmed_authors>Huang M</pubmed_authors><pubmed_authors>Wei X</pubmed_authors><pubmed_authors>Wang W</pubmed_authors><pubmed_authors>Wang X</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Wu Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Evaluation of the transverse aortic constriction model in ICR and C57BL/6J mice.</name><description>Transverse aortic constriction (TAC) is a frequently used model to investigate pressure overload-induced progressive heart failure (HF); however, there is considerable phenotypic variation among different mouse strains and even sub-strains. Moreover, less is known about the TAC model in ICR mice. Therefore, to determine the suitability of the ICR strain for TAC-induced HF research, we compared the effects of TAC on ICR and C57BL/6J mice at one, two and four weeks post-TAC &lt;i>via&lt;/i> echocardiography, organ index, morphology, and histology. At the end of the study, behavior and gene expression patterns were assessed, and overall survival was monitored. Compared to the sham-operated mice, ICR and C57BL/6J mice displayed hypertrophic phenotypes with a significant increase in ventricle wall thickness, heart weight and ratio, and cross-sectional area of cardiomyocytes after a 2-week TAC exposure. In addition, ICR mice developed reduced systolic function and severe lung congestion 4 weeks post-TAC, whereas C57BL/6J did not. Besides, ICR mice demonstrated comparable survival, similar gene expression alteration but severer fibrotic remodeling and poor behavioral performance compared to the C57BL/6J mice. Our data demonstrated that ICR was quite sensitive to TAC-induced heart failure and can be an ideal research tool to investigate mechanisms and drug intervention for pressure overload-induced HF.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2025-04-04T19:49:48.343Z</modification><creation>2025-04-04T19:49:48.343Z</creation></dates><accession>S-EPMC9745147</accession><cross_references><pubmed>36523549</pubmed><doi>10.3389/fphys.2022.1026884</doi></cross_references></HashMap>