ArticleInternational journal of molecular sciences2015
Low T3 State Is Correlated with Cardiac Mitochondrial Impairments after Ischemia Reperfusion Injury: Evidence from a Proteomic Approach.
Article in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Inflammatory and hormonal crosstalk linking rheumatic fever to chronic valvular heart disease.Molecular biology reports · 2026Review
- The Relationship Between Pituitary Axis Hormones and All-Cause Mortality in Hospitalized Patients with Chronic Diseases: A Prospective Cohort Study.Medicina (Kaunas, Lithuania) · 2026Observational
- Analysis of Risk Factors for Major Adverse Cardiovascular Events in Patients with Coronary Stent Restenosis after Revascularization.Reviews in cardiovascular medicine · 2023Article
- Identification of Hub Genes in the Remodeling of Non-Infarcted Myocardium Following Acute Myocardial Infarction.Journal of cardiovascular development and disease · 2022Article
- Triiodothyronine (T3), inflammation and mortality risk in patients with acute myocardial infarction.European thyroid journal · 2022Article
- Thyroid Stimulating Hormone Triggers Hepatic Mitochondrial Stress through Cyclophilin D Acetylation.Oxidative medicine and cellular longevity · 2020Article
- Protective Effects of Euthyroidism Restoration on Mitochondria Function and Quality Control in Cardiac Pathophysiology.International journal of molecular sciences · 2019Review
- Review
- Cardioprotection and thyroid hormones.Heart failure reviews · 2016Review
- Mitochondria in Ageing and Diseases: The Super Trouper of the Cell.International journal of molecular sciences · 2016Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria are major determinants of cell fate in ischemia/reperfusion injury (IR) and common effectors of cardio-protective strategies in cardiac ischemic disease. Thyroid hormone homeostasis critically affects mitochondrial function and energy production. Since a low T3 state (LT3S) is frequently observed in the post infarction setting, the study was aimed to investigate the relationship between 72 h post IR T3 levels and both the cardiac function and the mitochondrial proteome in a rat model of IR. The low T3 group exhibits the most compromised cardiac performance along with the worst mitochondrial activity. Accordingly, our results show a different remodeling of the mitochondrial proteome in the presence or absence of a LT3S, with alterations in groups of proteins that play a key role in energy metabolism, quality control and regulation of cell death pathways. Overall, our findings highlight a relationship between LT3S in the early post IR and poor cardiac and mitochondrial outcomes, and suggest a potential implication of thyroid hormone in the cardio-protection and tissue remodeling in ischemic disease.
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Registered trials
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