Autophagy signaling in hypertrophied muscles of diabetic and control rats.

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dc.citation.issue9
dc.citation.volume13
dc.contributor.authorScervino MVM
dc.contributor.authorFortes MAS
dc.contributor.authorVitzel KF
dc.contributor.authorde Souza DR
dc.contributor.authorMurata GM
dc.contributor.authorSantana GO
dc.contributor.authorda Silva EB
dc.contributor.authorLevada-Pires AC
dc.contributor.authorKuwabara WMT
dc.contributor.authorLoureiro TCA
dc.contributor.authorCuri R
dc.contributor.editorKrützfeldt J
dc.coverage.spatialEngland
dc.date.accessioned2024-06-18T20:08:00Z
dc.date.available2024-06-18T20:08:00Z
dc.date.issued2023-07-20
dc.description.abstractAutophagy 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 days of overload hypertrophy in the extensor digitorum longus (EDL) and soleus muscles of control and diabetic rats. We compared control and 3-day streptozotocin-induced 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-induced hypertrophy or the levels of autophagy signaling proteins (p-ULK1, Beclin-1, Atg5, Atg12-5, Atg7, Atg3, LC3-I and II, and p62) in either muscle. The p-ULK-1, Beclin-1, 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-induced hypertrophy, with increases in Beclin-1, Atg5, Atg12-5, Atg7, Atg3, and LC3-I expression in the control and diabetic groups, in addition to p-ULK-1 in the control groups. After hypertrophy, Beclin-1 and Atg5 levels increased in the EDL muscle of both groups, while p-ULK1 and LC3-I 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-induced hypertrophy and autophagy signaling proteins in EDL and soleus muscles, with the two groups exhibiting different patterns of autophagy activation.
dc.description.confidentialfalse
dc.edition.editionSep 2023
dc.format.pagination1709-1722
dc.identifier.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/37470707
dc.identifier.citationScervino MVM, Fortes MAS, Vitzel KF, de Souza DR, Murata GM, Santana GO, da Silva EB, Levada-Pires AC, Kuwabara WMT, Loureiro TCA, Curi R. (2023). Autophagy signaling in hypertrophied muscles of diabetic and control rats.. FEBS Open Bio. 13. 9. (pp. 1709-1722).
dc.identifier.doi10.1002/2211-5463.13677
dc.identifier.eissn2211-5463
dc.identifier.elements-typejournal-article
dc.identifier.issn2211-5463
dc.identifier.urihttps://mro.massey.ac.nz/handle/10179/69888
dc.languageeng
dc.publisherJohn Wiley and Sons Ltd on behalf of Federation of European Biochemical Societies.
dc.publisher.urihttps://febs.onlinelibrary.wiley.com/doi/10.1002/2211-5463.13677
dc.relation.isPartOfFEBS Open Bio
dc.rights(c) 2023 The Author/s
dc.rightsCC BY 4.0
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectautolysosome
dc.subjectautophagosome
dc.subjectautophagy-related genes
dc.subjecthyperglycemia
dc.subjectprotein degradation
dc.subjectRats
dc.subjectAnimals
dc.subjectBeclin-1
dc.subjectDiabetes Mellitus, Experimental
dc.subjectMuscle, Skeletal
dc.subjectHypertrophy
dc.subjectAutophagy
dc.titleAutophagy signaling in hypertrophied muscles of diabetic and control rats.
dc.typeJournal article
pubs.elements-id478967
pubs.organisational-groupCollege of Health
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