{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T22:30:00Z","timestamp":1792621800607,"version":"4.5.0"},"reference-count":45,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2021,5,6]],"date-time":"2021-05-06T00:00:00Z","timestamp":1620259200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81672218"],"award-info":[{"award-number":["81672218"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82072436"],"award-info":[{"award-number":["82072436"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81900797"],"award-info":[{"award-number":["81900797"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100009075","name":"Guangdong Academy of Sciences","doi-asserted-by":"publisher","award":["2018GDASCX\u20100806"],"award-info":[{"award-number":["2018GDASCX\u20100806"]}],"id":[{"id":"10.13039\/501100009075","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100009075","name":"Guangdong Academy of Sciences","doi-asserted-by":"publisher","award":["2018GDASCX\u20100102"],"award-info":[{"award-number":["2018GDASCX\u20100102"]}],"id":[{"id":"10.13039\/501100009075","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100009075","name":"Guangdong Academy of Sciences","doi-asserted-by":"publisher","award":["2016GDASRC\u20100202"],"award-info":[{"award-number":["2016GDASRC\u20100202"]}],"id":[{"id":"10.13039\/501100009075","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J cachexia sarcopenia muscle"],"published-print":{"date-parts":[[2021,6]]},"abstract":"Abstract<\/jats:title>\n \n Background<\/jats:title>\n \n Satellite cells (SCs) are critical to skeletal muscle regeneration. Inactivation of SCs is linked to skeletal muscle loss. Transferrin receptor 1 (Tfr1) is associated with muscular dysfunction as muscle\u2010specific deletion of\n Tfr1<\/jats:italic>\n results in growth retardation, metabolic disorder, and lethality, shedding light on the importance of Tfr1 in muscle physiology. However, its physiological function regarding skeletal muscle ageing and regeneration remains unexplored.\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n RNA sequencing is applied to skeletal muscles of different ages to identify Tfr1 associated to skeletal muscle ageing. Mice with conditional SC ablation of\n Tfr1<\/jats:italic>\n were generated. Between\n Tfr1<\/jats:italic>\n \n SC\/WT<\/jats:italic>\n <\/jats:sup>\n and\n Tfr1<\/jats:italic>\n \n SC\/KO<\/jats:italic>\n <\/jats:sup>\n (\n n<\/jats:italic>\n \u00a0=\u00a06\u20138 mice per group), cardiotoxin was intramuscularly injected, and transverse abdominal muscle was dissected, weighted, and cryosectioned, followed by immunostaining, haematoxylin and eosin staining, and Masson staining. These phenotypical analyses were followed with functional analysis such as flow cytometry, tread mill, Prussian blue staining, and transmission electron microscopy to identify pathological pathways that contribute to regeneration defects.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n By comparing gene expression between young (2\u00a0weeks old,\n n<\/jats:italic>\n \u00a0=\u00a03) and aged (80\u00a0weeks old,\n n<\/jats:italic>\n \u00a0=\u00a03) mice among four types of muscles, we identified that\n Tfr1<\/jats:italic>\n expression is declined in muscles of aged mice (~80% reduction,\n P<\/jats:italic>\n \u00a0<\u00a00.005), so as to its protein level in SCs of aged mice. From\n in vivo<\/jats:italic>\n and\n ex vivo<\/jats:italic>\n experiments,\n Tfr1<\/jats:italic>\n deletion in SCs results in an irreversible depletion of SCs (~60% reduction,\n P<\/jats:italic>\n \u00a0<\u00a00.005) and cell\u2010autonomous defect in SC proliferation and differentiation, leading to skeletal muscle regeneration impairment, followed by labile iron accumulation, lipogenesis, and decreased Gpx4 and Nrf2 protein levels leading to reactive oxygen species scavenger defects. These abnormal phenomena including iron accumulation, activation of unsaturated fatty acid biosynthesis, and lipid peroxidation are orchestrated with the occurrence of ferroptosis in skeletal muscle. Ferroptosis further exacerbates SC proliferation and skeletal muscle regeneration. Ferrostatin\u20101, a ferroptosis inhibitor, could not rescue ferroptosis. However, intramuscular administration of lentivirus\u2010expressing Tfr1 could partially reduce labile iron accumulation, decrease lipogenesis, and promote skeletal muscle regeneration. Most importantly, declined Tfr1 but increased Slc39a14 protein level on cellular membrane contributes to labile iron accumulation in skeletal muscle of aged rodents (~80\u00a0weeks old), leading to activation of ferroptosis in aged skeletal muscle. This is inhibited by ferrostatin\u20101 to improve running time (\n P<\/jats:italic>\n \u00a0=\u00a00.0257) and distance (\n P<\/jats:italic>\n \u00a0=\u00a00.0248).\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n Satellite cell\u2010specific deletion of\n Tfr1<\/jats:italic>\n impairs skeletal muscle regeneration with activation of ferroptosis. This phenomenon is recapitulated in skeletal muscle of aged rodents and human sarcopenia. Our study provides mechanistic information for developing novel therapeutic strategies against muscular ageing and diseases.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1002\/jcsm.12700","type":"journal-article","created":{"date-parts":[[2021,5,6]],"date-time":"2021-05-06T21:40:01Z","timestamp":1620337201000},"page":"746-768","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":185,"title":["Transferrin receptor 1 ablation in satellite cells impedes skeletal muscle regeneration through activation of ferroptosis"],"prefix":"10.1002","volume":"12","author":[{"given":"Hongrong","family":"Ding","sequence":"first","affiliation":[{"name":"Guangdong Provincial Key Laboratory of Microbial Culture Collection and Application, State Key Laboratory of Applied Microbiology Southern China Institute of Microbiology, Guangdong Academy of Sciences Guangzhou China"},{"name":"Guangdong Provincial Key Laboratory of Molecular Diagnosis, The Marine 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