<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>21(2)</volume><submitter>Unten Y</submitter><pubmed_abstract>Age-associated declines in skeletal muscle function are linked to cellular senescence and mitochondrial alterations, yet mitochondrial phenotypes in aged human myoblasts remain insufficiently characterized. Here, we examined primary skeletal muscle myoblasts from young and elderly donors to assess mitochondrial function, morphology, and mitochondria-endoplasmic reticulum (ER) contact sites (MERCS). Myoblasts from older donors exhibited senescence features, including elevated SA-β-gal activity and reduced Lamin B1 expression, accompanied by increased mitochondrial oxidative stress. Despite marked mitochondrial hyperfusion and increased mitochondrial DNA content, mitochondrial oxygen consumption rate and membrane potential per mitochondrial area were comparable between young and old cells. M</pubmed_abstract><journal>PloS one</journal><pagination>e0343604</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12923047</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Characterizing mitochondrial phenotypes and MERCS in aged human skeletal muscle myoblasts.</pubmed_title><pmcid>PMC12923047</pmcid><pubmed_authors>Tateishi N</pubmed_authors><pubmed_authors>Shiiba I</pubmed_authors><pubmed_authors>Yanagi S</pubmed_authors><pubmed_authors>Suzuki T</pubmed_authors><pubmed_authors>Unten Y</pubmed_authors><pubmed_authors>Masukagami Y</pubmed_authors><pubmed_authors>Husnik F</pubmed_authors><pubmed_authors>Horiuchi K</pubmed_authors><pubmed_authors>Takafuji K</pubmed_authors></additional><is_claimable>false</is_claimable><name>Characterizing mitochondrial phenotypes and MERCS in aged human skeletal muscle myoblasts.</name><description>Age-associated declines in skeletal muscle function are linked to cellular senescence and mitochondrial alterations, yet mitochondrial phenotypes in aged human myoblasts remain insufficiently characterized. Here, we examined primary skeletal muscle myoblasts from young and elderly donors to assess mitochondrial function, morphology, and mitochondria-endoplasmic reticulum (ER) contact sites (MERCS). Myoblasts from older donors exhibited senescence features, including elevated SA-β-gal activity and reduced Lamin B1 expression, accompanied by increased mitochondrial oxidative stress. Despite marked mitochondrial hyperfusion and increased mitochondrial DNA content, mitochondrial oxygen consumption rate and membrane potential per mitochondrial area were comparable between young and old cells. M</description><dates><release>2026-01-01T00:00:00Z</release><publication>2026</publication><modification>2026-07-16T12:27:46.861Z</modification><creation>2026-07-09T10:54:07.453Z</creation></dates><accession>S-EPMC12923047</accession><cross_references><pubmed>41719251</pubmed><doi>10.1371/journal.pone.0343604</doi></cross_references></HashMap>