<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Oh J</submitter><funding>National Research Foundation of Korea</funding><pagination>1945</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12731566</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(24)</volume><pubmed_abstract>Osteoporosis is a major global health challenge, causing millions of fragility fractures each year and imposing an escalating socioeconomic burden worldwide. Despite advances with antiresorptive and anabolic therapies, substantial residual fracture risk persists, and targeting aging biology may yield disease modifying benefits beyond current standards of care. Senescent cells secrete senescence-associated secretory phenotype (SASP) factors, which impair osteoblast differentiation and contribute to bone loss. We investigated foretinib, a quinoline-based multi-tyrosine kinase inhibitor, as a potential anti-aging agent in osteoblast lineage cells. Foretinib inhibited doxorubicin-induced senescence in osteoblast progenitors via the p53/p21 and p16 pathways and reduced the expression of osteoge</pubmed_abstract><journal>Cells</journal><pubmed_title>Foretinib Alleviates Osteoblast Senescence and Protects Against Bone Loss in Ovariectomized Mice by Promoting Osteoblast Differentiation.</pubmed_title><pmcid>PMC12731566</pmcid><funding_grant_id>RS-2022-NR070844; RS-2022-NR068998</funding_grant_id><pubmed_authors>Kim T</pubmed_authors><pubmed_authors>Ha H</pubmed_authors><pubmed_authors>Oh J</pubmed_authors><pubmed_authors>Jeong D</pubmed_authors><pubmed_authors>Lee J</pubmed_authors><pubmed_authors>Lee K</pubmed_authors><pubmed_authors>Kim EC</pubmed_authors><pubmed_authors>Kim JR</pubmed_authors></additional><is_claimable>false</is_claimable><name>Foretinib Alleviates Osteoblast Senescence and Protects Against Bone Loss in Ovariectomized Mice by Promoting Osteoblast Differentiation.</name><description>Osteoporosis is a major global health challenge, causing millions of fragility fractures each year and imposing an escalating socioeconomic burden worldwide. Despite advances with antiresorptive and anabolic therapies, substantial residual fracture risk persists, and targeting aging biology may yield disease modifying benefits beyond current standards of care. Senescent cells secrete senescence-associated secretory phenotype (SASP) factors, which impair osteoblast differentiation and contribute to bone loss. We investigated foretinib, a quinoline-based multi-tyrosine kinase inhibitor, as a potential anti-aging agent in osteoblast lineage cells. Foretinib inhibited doxorubicin-induced senescence in osteoblast progenitors via the p53/p21 and p16 pathways and reduced the expression of osteoge</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Dec</publication><modification>2026-05-26T20:07:43.606Z</modification><creation>2026-05-25T03:11:38.247Z</creation></dates><accession>S-EPMC12731566</accession><cross_references><pubmed>41439965</pubmed><doi>10.3390/cells14241945</doi></cross_references></HashMap>