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Title: Melatonin/Nrf2/NLRP3 Connection in Mouse Heart Mitochondria during Aging
Authors: Fernández-Ortiz, Marisol
Sayed, Ramy K.A.
Fernández-Martínez, José
Cionfrini, Antonia
Aranda-Martínez, Paula
Escames, Germaine
de Haro, Tomás
Acuña-Castroviejo, Darío
metadata.dc.contributor.authoraffiliation: [Fernández-Ortiz,M; Sayed,RKA; Fernández-Martínez,J; Cionfrini,A; Aranda-Martínez,P; Escames,G; Acuña-Castroviejo,D] Centro de Investigación Biomédica, Departamento de Fisiología, Facultad de Medicina, Instituto de Biotecnología, Parque Tecnológico de Ciencias de la Salud, Universidad de Granada, Granada, Spain. [Sayed,RKA] Department of Anatomy and Embryology, Faculty of Veterinary Medicine, Sohag University, Sohag, Egypt. [Escames,G; Acuña-Castroviejo,D] CIBERfes, Ibs. Granada, Granada, Spain. [de Haro,T; Acuña-Castroviejo,D] UGC de Laboratorios Clínicos, Hospital Universitario San Cecilio, Granada, Spain.
Keywords: Melatonin;Mitochondria;NLRP3 inflammasome;Nrf2;Heart ultrastructure;Apoptosis;Mitochondrial dynamics;Melatonina;Mitocondria;Corazón;Inflamasomas;Factor 2 Relacionado con NF-E2
metadata.dc.subject.mesh: Medical Subject Headings::Chemicals and Drugs::Hormones, Hormone Substitutes, and Hormone Antagonists::Hormones::Melatonin
Medical Subject Headings::Anatomy::Cells::Cellular Structures::Subcellular Fractions::Mitochondria
Medical Subject Headings::Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Death::Apoptosis
Medical Subject Headings::Organisms::Eukaryota::Animals
Medical Subject Headings::Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Rodentia::Muridae::Murinae::Mice
Medical Subject Headings::Chemicals and Drugs::Macromolecular Substances::Multiprotein Complexes::Inflammasomes
Medical Subject Headings::Chemicals and Drugs::Amino Acids, Peptides, and Proteins::Proteins::DNA-Binding Proteins::Basic-Leucine Zipper Transcription Factors::NF-E2-Related Factor 2
Medical Subject Headings::Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Molecular Mechanisms of Pharmacological Action::Antioxidants
Medical Subject Headings::Diseases::Cardiovascular Diseases
Medical Subject Headings::Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Death::Autophagy
Medical Subject Headings::Phenomena and Processes::Physiological Phenomena::Physiological Processes::Growth and Development::Aging
Medical Subject Headings::Phenomena and Processes::Physiological Phenomena::Physiological Processes::Stress, Physiological::Oxidative Stress
Issue Date: 27-Nov-2020
Publisher: MDPI
Citation: Fernández-Ortiz M, Sayed RKA, Fernández-Martínez J, Cionfrini A, Aranda-Martínez P, Escames G, et al. Melatonin/Nrf2/NLRP3 Connection in Mouse Heart Mitochondria during Aging. Antioxidants. 2020 Nov 27;9(12):1187
Abstract: Aging is a major risk for cardiovascular diseases (CVD). Age-related disorders include oxidative stress, mitochondria dysfunction, and exacerbation of the NF-κB/NLRP3 innate immune response pathways. Some of the molecular mechanisms underlying these processes, however, remain unclear. This study tested the hypothesis that NLRP3 inflammasome plays a role in cardiac aging and melatonin is able to counteract its effects. With the aim of investigating the impact of NLRP3 inflammasome and the actions and target of melatonin in aged myocardium, we analyzed the expression of proteins implied in mitochondria dynamics, autophagy, apoptosis, Nrf2-dependent antioxidant response and mitochondria ultrastructure in heart of wild-type and NLRP3-knockout mice of 3, 12, and 24 months-old, with and without melatonin treatment. Our results showed that the absence of NLRP3 prevented age-related mitochondrial dynamic alterations in cardiac muscle with minimal effects in cardiac autophagy during aging. The deficiency of the inflammasome affected Bax/Bcl2 ratio, but not p53 or caspase 9. The Nrf2-antioxidant pathway was also unaffected by the absence of NLRP3. Furthermore, NLRP3-deficiency prevented the drop in autophagy and mice showed less mitochondrial damage than wild-type animals. Interestingly, melatonin treatment recovered mitochondrial dynamics altered by aging and had few effects on cardiac autophagy. Melatonin supplementation also had an anti-apoptotic action in addition to restoring Nrf2-antioxidant capacity and improving mitochondria ultrastructure altered by aging.
metadata.dc.identifier.doi: 10.3390/antiox9121187
ISSN: 2076-3921 (Online)
Appears in Collections:01- Artículos - Hospital San Cecilio
01- Artículos - ibsGRANADA. Instituto de Investigación Biosanitaria de Granada

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