ArticlePloS one2013
Thyroid hormone reverses aging-induced myocardial fatty acid oxidation defects and improves the response to acutely increased afterload.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- The effect of enhanced glycolysis on cardiac aging.GeroScience · 2025Article
- Sex impacts cardiac function and the proteome response to thyroid hormone in aged mice.Proteome science · 2020Article
- Mitochondria and Calcium Homeostasis: Cisd2 as a Big Player in Cardiac Ageing.International journal of molecular sciences · 2020Review
- First characterization of glucose flux through the hexosamine biosynthesis pathway (HBP) inThe Journal of biological chemistry · 2020Article
- O-GlcNAc Transferase Promotes Compensated Cardiac Function and Protein Kinase A O-GlcNAcylation During Early and Established Pathological Hypertrophy From Pressure Overload.Journal of the American Heart Association · 2019Article
- Mitochondrial Metabolism in Aging Heart.Circulation research · 2016Review
- Assessing Cardiac Metabolism: A Scientific Statement From the American Heart Association.Circulation research · 2016Review
- Role of thyroid hormones in ventricular remodeling.Current heart failure reports · 2015Review
- Article
- Triiodothyronine facilitates weaning from extracorporeal membrane oxygenation by improved mitochondrial substrate utilization.Journal of the American Heart Association · 2014Article
- Is the lack of adiponectin associated with increased ER/SR stress and inflammation in the heart?Adipocyte · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundSubclinical hypothyroidism occurs during aging in humans and mice and may contribute to the development of heart failure. Aging also impairs myocardial fatty acid oxidation, causing increased reliance on flux through pyruvate dehydrogenase (PDH) to maintain function. We hypothesize that the metabolic changes in aged hearts make them less tolerant to acutely increased work and that thyroid hormone supplementation reverses these defects.
methodsStudies were performed on young (Young, 4-6 months) and aged (Old, 22-24 months) C57/BL6 mice at standard (50 mmHg) and high afterload (80 mmHg). Another aged group received thyroid hormone for 3 weeks (Old-TH, high afterload only). Function was measured in isolated working hearts along with substrate fractional contributions (Fc) to the citric acid cycle (CAC) using perfusate with (13)C labeled lactate, pyruvate, glucose and unlabeled palmitate and insulin.
resultsOld mice maintained cardiac function under standard workload conditions, despite a marked decrease in unlabeled (presumably palmitate) Fc and relatively similar individual carbohydrate contributions. However, old mice exhibited reduced palmitate oxidation with diastolic dysfunction exemplified by lower -dP/dT. Thyroid hormone abrogated the functional and substrate flux abnormalities in aged mice.
conclusionThe aged heart shows diminished ability to increase cardiac work due to substrate limitations, primarily impaired fatty acid oxidation. The heart accommodates slightly by increasing efficiency through oxidation of carbohydrate substrates. Thyroid hormone supplementation in aged mice significantly improves cardiac function potentially through restoration of fatty acid oxidation.
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