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dc.contributor.authorSayed, Ramy K. A.
dc.contributor.authorFernández Ortiz, Marisol
dc.contributor.authorFernández Martínez, José 
dc.contributor.authorAranda Martínez, Paula 
dc.contributor.authorRusanova Rusanova, Iryna 
dc.contributor.authorMartínez Ruiz, Laura 
dc.contributor.authorEscames Rosa, Germaine 
dc.contributor.authorAcuña Castroviejo, Darío 
dc.date.accessioned2021-10-05T10:36:58Z
dc.date.available2021-10-05T10:36:58Z
dc.date.issued2021-08-10
dc.identifier.citationSayed, R.K.A... [et al.]. The Impact of Melatonin Supplementation and NLRP3 Inflammasome Deletion on Age-Accompanied Cardiac Damage. Antioxidants 2021, 10, 1269. [https://doi.org/10.3390/antiox10081269]es_ES
dc.identifier.urihttp://hdl.handle.net/10481/70647
dc.descriptionThis study was partially supported by grants from the Instituto de Salud Carlos III through the projects PI13-981, PI16-00519, PI19-01372, and CB/10/00238 (Co-funded by European Regional Development Fund/European Social Fund "Investing in your future"); the Conserjeria de Economia, Innovacion, Ciencia y Empleo, Junta de Andalucia (CTS-101), Spain, and also by Sohag University, Egypt. M.F.-O and J.F.-M are supported by a FPU fellowship from the Ministerio de Educacion, Spain.es_ES
dc.description.abstractTo investigate the role of NLRP3 inflammasome in cardiac aging, we evaluate here morphological and ultrastructural age-related changes of cardiac muscles fibers in wild-type and NLRP3-knockout mice, as well as studying the beneficial effect of melatonin therapy. The results clarified the beginning of the cardiac sarcopenia at the age of 12 months, with hypertrophy of cardiac myocytes, increased expression of beta-MHC, appearance of small necrotic fibers, decline of cadiomyocyte number, destruction of mitochondrial cristae, appearance of small-sized residual bodies, and increased apoptotic nuclei ratio. These changes were progressed in the cardiac myocytes of 24 old mice, accompanied by excessive collagen deposition, higher expressions of IL-1 alpha, IL-6, and TNF alpha, complete mitochondrial vacuolation and damage, myofibrils disorganization, multivesicular bodies formation, and nuclear fragmentation. Interestingly, cardiac myocytes of NLRP3(-/-) mice showed less detectable age-related changes compared with WT mice. Oral melatonin therapy preserved the normal cardiomyocytes structure, restored cardiomyocytes number, and reduced beta-MHC expression of cardiac hypertrophy. In addition, melatonin recovered mitochondrial architecture, reduced apoptosis and multivesicular bodies' formation, and decreased expressions of beta-MHC, IL-1 alpha, and IL-6. Fewer cardiac sarcopenic changes and highly remarkable protective effects of melatonin treatment detected in aged cardiomyocytes of NLRP3(-/-) mice compared with aged WT animals, confirming implication of the NLRP3 inflammasome in cardiac aging. Thus, NLRP3 suppression and melatonin therapy may be therapeutic approaches for age-related cardiac sarcopenia.es_ES
dc.description.sponsorshipInstituto de Salud Carlos III (European Regional Development Fund/European Social Fund "Investing in your future") PI13-981 PI16-00519 PI19-01372 CB/10/00238es_ES
dc.description.sponsorshipJunta de Andalucia CTS-101es_ES
dc.description.sponsorshipSohag Universityes_ES
dc.description.sponsorshipGerman Research Foundation (DFG)es_ES
dc.language.isoenges_ES
dc.publisherMDPIes_ES
dc.rightsAtribución 3.0 España*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.subjectCardiomyocyteses_ES
dc.subjectNLRP3-inflammasomees_ES
dc.subjectMitochondriaes_ES
dc.subjectCSAes_ES
dc.subjectUltrastructurees_ES
dc.subjectSarcopeniaes_ES
dc.subjectMelatonines_ES
dc.subjectAutophagosomees_ES
dc.subjectBeta-MHCes_ES
dc.titleThe Impact of Melatonin Supplementation and NLRP3 Inflammasome Deletion on Age-Accompanied Cardiac Damagees_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES
dc.identifier.doi10.3390/antiox10081269
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersiones_ES


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Atribución 3.0 España
Except where otherwise noted, this item's license is described as Atribución 3.0 España