ArticleAntioxidants (Basel, Switzerland)2021
The Impact of Melatonin Supplementation and NLRP3 Inflammasome Deletion on Age-Accompanied Cardiac Damage.
Article in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed.
- Progress in understanding how clock genes regulate aging and associated metabolic processes.Frontiers in physiology · 2025Review
- Chronobiotic and cytoprotective activity of melatonin in the cardiovascular system. Doses matter.Npj biological timing and sleep · 2024Review
- Melatonin and Vascular Function.Antioxidants (Basel, Switzerland) · 2024Review
- From Chronodisruption to Sarcopenia: The Therapeutic Potential of Melatonin.Biomolecules · 2023Review
- Age and Chronodisruption in Mouse Heart: Effect of the NLRP3 Inflammasome and Melatonin Therapy.International journal of molecular sciences · 2022Article
- Effect of Antioxidant Therapy on Oxidative Stress In Vivo 2021.Antioxidants (Basel, Switzerland) · 2022Article
- A Review of the Potential Effects of Melatonin in Compromised Mitochondrial Redox Activities in Elderly Patients With COVID-19.Frontiers in nutrition · 2022Review
- Melatonin as an Anti-Aging Therapy for Age-Related Cardiovascular and Neurodegenerative Diseases.Frontiers in aging neuroscience · 2022Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
To 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 β-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-1α, IL-6, and TNFα, complete mitochondrial vacuolation and damage, myofibrils disorganization, multivesicular bodies formation, and nuclear fragmentation. Interestingly, cardiac myocytes of NLRP3
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Registered trials
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