Dietary magnesium supplementation improves lifespan in a mouse model of progeria
Villa-Bellosta R
EMBO molecular medicine · 50 citations
How it was studied
- Design
- Animal study (classified by our AI screen)
- Studied in
- Animals
- Main outcome
- Clinical events such as disease or death
Who paid for it
- Funding
- Independent funding
- Nonprofit
- Progeria Research Foundation
- Government
- Ministerio de Asuntos Económicos y Transformación Digital, Gobierno de España
- Government
- Ministerio de Economía, Industria y Competitividad, Gobierno de España
- Government
- Ministerio de Economía, Industria y Competitividad, Gobierno de España (MINECO)
- Grants
- Progeria Research Foundation (PRF-2016-68); Ministerio de Asuntos Económicos y Transformación Digital, Gobierno de España (SAF‐2014-60669‐JIN)
Based on 4 listed funder(s) and full-text disclosure statement.
Publication
- Published
- 2020-08-16 · EMBO Mol Med · vol. 12 · issue 10 · p. e12423
- Publisher
- Springer Nature
- Cited
- 61 citations · more than 90% of similar papers · 2.4× the field average
- Impact
- Top 10% most cited in its field
- References
- 65 works
- Access
- Open access (journal) · CC-BY
- Research areas
- Nuclear Structure and Function · Birth, Development, and Health · Mitochondrial Function and Pathology
- Keywords
- Progeria, Magnesium, Medicine, Endocrinology, Internal medicine, Gerontology, Biology, Chemistry, Biochemistry, Gene
- MeSH
- animals, humans, mice, progeria, disease models, animal, magnesium, longevity, dietary supplements
1 author
From ES
- Ricardo Villa‐Bellosta · correspondingHospital Universitario Fundación Jiménez Díaz; Instituto de Investigación Sanitaria Fundación Jiménez Díaz; Universidad Autónoma de Madrid
Abstract
Aging is associated with redox imbalance according to the redox theory of aging. Consistently, a mouse model of premature aging (LmnaG609G/+ ) showed an increased level of mitochondrial reactive oxygen species (ROS) and a reduced basal antioxidant capacity, including loss of the NADPH-coupled glutathione redox system. LmnaG609G/+ mice also exhibited reduced mitochondrial ATP synthesis secondary to ROS-induced mitochondrial dysfunction. Treatment of LmnaG609G/+ vascular smooth muscle cells with magnesium-enriched medium improved the intracellular ATP level, enhanced the antioxidant capacity, and thereby reduced mitochondrial ROS production. Moreover, treatment of LmnaG609G/+ mice with dietary magnesium improved the proton pumps (complexes I, III, and IV), stimulated extramitochondrial NADH oxidation and enhanced the coupled mitochondrial membrane potential, and thereby increased H+ -coupled mitochondrial NADPH and ATP synthesis, which is necessary for cellular energy supply and survival. Consistently, magnesium treatment reduced calcification of vascular smooth muscle cells in vitro and in vivo, and improved the longevity of mice. This antioxidant property of magnesium may be beneficial in children with HGPS.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY).
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