{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,12]],"date-time":"2025-12-12T13:45:17Z","timestamp":1765547117283,"version":"3.40.5"},"reference-count":63,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2023,7,26]],"date-time":"2023-07-26T00:00:00Z","timestamp":1690329600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100003593","name":"Conselho Nacional de Desenvolvimento Cient\u00edfico e Tecnol\u00f3gico","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100003593","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002322","name":"Coordena\u00e7\u00e3o de Aperfei\u00e7oamento de Pessoal de N\u00edvel Superior","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100002322","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001807","name":"Funda\u00e7\u00e3o de Amparo \u00e0 Pesquisa do Estado de S\u00e3o Paulo","doi-asserted-by":"publisher","award":["2016\/11661\u20106","2016\/15766\u20107","2019\/02175\u20109","2019\/19097\u20100","2020\/00707\u20100"],"award-info":[{"award-number":["2016\/11661\u20106","2016\/15766\u20107","2019\/02175\u20109","2019\/19097\u20100","2020\/00707\u20100"]}],"id":[{"id":"10.13039\/501100001807","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["febs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["FEBS Open Bio"],"published-print":{"date-parts":[[2023,9]]},"abstract":"<jats:p>Autophagy plays a vital role in cell homeostasis by eliminating nonfunctional components and promoting cell survival. Here, we examined the levels of autophagy signaling proteins after 7\u2009days of overload hypertrophy in the extensor digitorum longus (EDL) and soleus muscles of control and diabetic rats. We compared control and 3\u2010day streptozotocin\u2010induced diabetic rats, an experimental model for type 1 diabetes mellitus (T1DM). EDL muscles showed increased levels of basal autophagy signaling proteins. The diabetic state did not affect the extent of overload\u2010induced hypertrophy or the levels of autophagy signaling proteins (p\u2010ULK1, Beclin\u20101, Atg5, Atg12\u20105, Atg7, Atg3, LC3\u2010I and II, and p62) in either muscle. The p\u2010ULK\u20101, Beclin\u20101, and p62 protein expression levels were higher in the EDL muscle than in the soleus before the hypertrophic stimulus. On the contrary, the soleus muscle exhibited increased autophagic signaling after overload\u2010induced hypertrophy, with increases in Beclin\u20101, Atg5, Atg12\u20105, Atg7, Atg3, and LC3\u2010I expression in the control and diabetic groups, in addition to p\u2010ULK\u20101 in the control groups. After hypertrophy, Beclin\u20101 and Atg5 levels increased in the EDL muscle of both groups, while p\u2010ULK1 and LC3\u2010I increased in the control group. In conclusion, the baseline EDL muscle exhibited higher autophagy than the soleus muscle. Although TDM1 promotes skeletal muscle mass loss and strength reduction, it did not significantly alter the extent of overload\u2010induced hypertrophy and autophagy signaling proteins in EDL and soleus muscles, with the two groups exhibiting different patterns of autophagy activation.<\/jats:p>","DOI":"10.1002\/2211-5463.13677","type":"journal-article","created":{"date-parts":[[2023,7,20]],"date-time":"2023-07-20T15:28:41Z","timestamp":1689866921000},"page":"1709-1722","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Autophagy signaling in hypertrophied muscles of diabetic and control rats"],"prefix":"10.1002","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5742-8820","authenticated-orcid":false,"given":"Maria V. 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