<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>12</volume><submitter>Li C</submitter><pubmed_abstract>&lt;h4>Introduction&lt;/h4>This study aimed to investigate the damaging effects of a high-fat diet (HFD) on mitochondria and skeletal muscle and to evaluate the protective role of astaxanthin (Asta), with a focus on mitochondrial biogenesis, oxidative stress, and inflammation under metabolic stress.&lt;h4>Methods&lt;/h4>HFD-fed mice and palmitate acid (PA)-stimulated C2C12 cells were treated with Asta. Skeletal muscle function, pathology, mitochondrial ultrastructure, inflammatory responses, and oxidative stress levels were assessed using behavioral tests, histology, quantitative reverse transcription-polymerase chain reaction, western blotting, transmission electron microscopy, and biochemical assays.&lt;h4>Results&lt;/h4>Asta did not alter body weight or serum lipid levels in HFD-fed mice but markedly alleviated skeletal muscle damage and improved function. In both &lt;i>in vivo&lt;/i> and &lt;i>in vitro&lt;/i> models, Asta suppressed inflammatory gene expression, enhanced mitochondrial biogenesis-related proteins, reduced lipid accumulation and mitochondrial damage, increased antioxidant enzyme activity, and promoted ATP production. Furthermore, Asta inhibited mitochondrial fission and lipid peroxidation in PA-stimulated C2C12 cells.&lt;h4>Discussion&lt;/h4>Asta mitigates oxidative stress, lipid accumulation, and inflammation in skeletal muscle cells by promoting mitochondrial biogenesis, thereby preserving muscle structure and function. These findings highlight Asta's potential as a therapeutic agent for skeletal muscle protection in metabolic stress conditions.</pubmed_abstract><journal>Frontiers in veterinary science</journal><pagination>1577408</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12439717</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Astaxanthin alleviates oxidative stress and skeletal muscle damage by promoting mitochondrial biogenesis.</pubmed_title><pmcid>PMC12439717</pmcid><pubmed_authors>Li C</pubmed_authors><pubmed_authors>Jiang T</pubmed_authors><pubmed_authors>Yan Y</pubmed_authors><pubmed_authors>Wang K</pubmed_authors></additional><is_claimable>false</is_claimable><name>Astaxanthin alleviates oxidative stress and skeletal muscle damage by promoting mitochondrial biogenesis.</name><description>&lt;h4>Introduction&lt;/h4>This study aimed to investigate the damaging effects of a high-fat diet (HFD) on mitochondria and skeletal muscle and to evaluate the protective role of astaxanthin (Asta), with a focus on mitochondrial biogenesis, oxidative stress, and inflammation under metabolic stress.&lt;h4>Methods&lt;/h4>HFD-fed mice and palmitate acid (PA)-stimulated C2C12 cells were treated with Asta. Skeletal muscle function, pathology, mitochondrial ultrastructure, inflammatory responses, and oxidative stress levels were assessed using behavioral tests, histology, quantitative reverse transcription-polymerase chain reaction, western blotting, transmission electron microscopy, and biochemical assays.&lt;h4>Results&lt;/h4>Asta did not alter body weight or serum lipid levels in HFD-fed mice but markedly alleviated skeletal muscle damage and improved function. In both &lt;i>in vivo&lt;/i> and &lt;i>in vitro&lt;/i> models, Asta suppressed inflammatory gene expression, enhanced mitochondrial biogenesis-related proteins, reduced lipid accumulation and mitochondrial damage, increased antioxidant enzyme activity, and promoted ATP production. Furthermore, Asta inhibited mitochondrial fission and lipid peroxidation in PA-stimulated C2C12 cells.&lt;h4>Discussion&lt;/h4>Asta mitigates oxidative stress, lipid accumulation, and inflammation in skeletal muscle cells by promoting mitochondrial biogenesis, thereby preserving muscle structure and function. These findings highlight Asta's potential as a therapeutic agent for skeletal muscle protection in metabolic stress conditions.</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025</publication><modification>2026-04-08T19:50:49.135Z</modification><creation>2026-04-08T14:35:09.94Z</creation></dates><accession>S-EPMC12439717</accession><cross_references><pubmed>40963587</pubmed><doi>10.3389/fvets.2025.1577408</doi></cross_references></HashMap>