<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>13</volume><submitter>Long K</submitter><pubmed_abstract>&lt;b>Background:&lt;/b> Heart failure, especially chronic heart failure, is generally induced by the accumulation of reactive oxygen species (ROS), as well as the subsequent loss of mitochondrial permeability transition pore (mPTP) openings and pathological mitochondrial dysfunction. Herein, we explored the therapeutic effects of the Chinese medicine Yangxin Keli (YXXKL) on chronic heart failure and its underlying working mechanism. &lt;b>Methods:&lt;/b> To mimic oxidative stress-induced chronic heart failure, a rat heart failure model was induced by the administration of DOX. Transthoracic echocardiography was performed to confirm the successful establishment of the heart failure model by observing significantly decreased cardiac function in the rats. Mitochondrial membrane potential, function, and </pubmed_abstract><journal>Frontiers in pharmacology</journal><pagination>931453</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9468485</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Yang-xin-xue keli exerts therapeutic effects &lt;i>via&lt;/i> regulating mitochondrial homeostasis and function in doxorubicin-induced rat heart failure.</pubmed_title><pmcid>PMC9468485</pmcid><pubmed_authors>Wang M</pubmed_authors><pubmed_authors>Zhi L</pubmed_authors><pubmed_authors>Gao P</pubmed_authors><pubmed_authors>Chen J</pubmed_authors><pubmed_authors>Wang C</pubmed_authors><pubmed_authors>Long K</pubmed_authors><pubmed_authors>Liao D</pubmed_authors><pubmed_authors>Zhao Z</pubmed_authors></additional><is_claimable>false</is_claimable><name>Yang-xin-xue keli exerts therapeutic effects &lt;i>via&lt;/i> regulating mitochondrial homeostasis and function in doxorubicin-induced rat heart failure.</name><description>&lt;b>Background:&lt;/b> Heart failure, especially chronic heart failure, is generally induced by the accumulation of reactive oxygen species (ROS), as well as the subsequent loss of mitochondrial permeability transition pore (mPTP) openings and pathological mitochondrial dysfunction. Herein, we explored the therapeutic effects of the Chinese medicine Yangxin Keli (YXXKL) on chronic heart failure and its underlying working mechanism. &lt;b>Methods:&lt;/b> To mimic oxidative stress-induced chronic heart failure, a rat heart failure model was induced by the administration of DOX. Transthoracic echocardiography was performed to confirm the successful establishment of the heart failure model by observing significantly decreased cardiac function in the rats. Mitochondrial membrane potential, function, and </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2025-04-22T03:26:15.645Z</modification><creation>2025-02-18T23:55:39.424Z</creation></dates><accession>S-EPMC9468485</accession><cross_references><pubmed>36110548</pubmed><doi>10.3389/fphar.2022.931453</doi></cross_references></HashMap>