<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Xinyi S</submitter><funding>Anhui Province Scientific Research Preparation Program Project</funding><funding>'Feng Yuan' Program</funding><pagination>e70141</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12657642</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(6)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Excessive fat accumulation in muscles with disuse atrophy may impair muscle physiologic function and exacerbate the progression of atrophy, with causes largely unexplored. Evidence indicates leptin plays a crucial role in regulating skeletal muscle fat metabolism. Masticatory muscle (a special skeletal muscle) atrophy often causes aesthetic and functional problems due to various occlusal factors. This study examines leptin's role and mechanism in masseter muscle disuse atrophy and explores leptin's source.&lt;h4>Methods&lt;/h4>A C57BL/6J mouse disuse atrophy model was established. The ameliorative role of leptin in masseter muscle lipid accumulation and atrophy and its local sources were explored by injection of exogenous leptin and nilotinib, which specifically induces leptin</pubmed_abstract><journal>Journal of cachexia, sarcopenia and muscle</journal><pubmed_title>Leptin From Fibro-Adipogenic Progenitor Cells (FAPs) Regulates Masseter Muscle Disuse Atrophy and Ectopic Fat Accumulation.</pubmed_title><pmcid>PMC12657642</pmcid><funding_grant_id>2022xkfyhz03</funding_grant_id><funding_grant_id>2022AH050734</funding_grant_id><funding_grant_id>2023xkfytszd02</funding_grant_id><pubmed_authors>Ang G</pubmed_authors><pubmed_authors>Yongfeng H</pubmed_authors><pubmed_authors>Tingting W</pubmed_authors><pubmed_authors>Qingchun L</pubmed_authors><pubmed_authors>Hao Y</pubmed_authors><pubmed_authors>Yuanyin W</pubmed_authors><pubmed_authors>Keke Z</pubmed_authors><pubmed_authors>Tingting L</pubmed_authors><pubmed_authors>Xinyi S</pubmed_authors><pubmed_authors>Xiaoyu L</pubmed_authors><pubmed_authors>Yi C</pubmed_authors><pubmed_authors>Yuhe C</pubmed_authors><pubmed_authors>Wei L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Leptin From Fibro-Adipogenic Progenitor Cells (FAPs) Regulates Masseter Muscle Disuse Atrophy and Ectopic Fat Accumulation.</name><description>&lt;h4>Background&lt;/h4>Excessive fat accumulation in muscles with disuse atrophy may impair muscle physiologic function and exacerbate the progression of atrophy, with causes largely unexplored. Evidence indicates leptin plays a crucial role in regulating skeletal muscle fat metabolism. Masticatory muscle (a special skeletal muscle) atrophy often causes aesthetic and functional problems due to various occlusal factors. This study examines leptin's role and mechanism in masseter muscle disuse atrophy and explores leptin's source.&lt;h4>Methods&lt;/h4>A C57BL/6J mouse disuse atrophy model was established. The ameliorative role of leptin in masseter muscle lipid accumulation and atrophy and its local sources were explored by injection of exogenous leptin and nilotinib, which specifically induces leptin</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Dec</publication><modification>2026-06-07T04:32:52.718Z</modification><creation>2026-06-07T03:06:55.13Z</creation></dates><accession>S-EPMC12657642</accession><cross_references><pubmed>41305914</pubmed><doi>10.1002/jcsm.70141</doi></cross_references></HashMap>