Trial reportRedox biology2018
Blocking mitochondrial cyclophilin D ameliorates TSH-impaired defensive barrier of artery.
Trial report in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- TSH promotes right ventricle hypertrophy and energy metabolism remodeling in PAH mice.Endocrine connections · 2025Article
- Integrative Mendelian randomization and multi-omics analysis identifies anti-allergic drug targets associated with cardiovascular disease risk.Scientific reports · 2025Article
- Thyroid Hormone Resistance Indices and Their Correlations With Insulin Resistance in Chinese Euthyroid Subjects.International journal of endocrinology · 2025Article
- The cyclophilin D (CypD) of Toxoplasma gondii is involved in the parasite's response to oxidative stress damage.Parasitology research · 2024Article
- PPARγ in Atherosclerotic Endothelial Dysfunction: Regulatory Compounds and PTMs.International journal of molecular sciences · 2023Review
- Natural Drugs: A New Direction for the Prevention and Treatment of Diabetes.Molecules (Basel, Switzerland) · 2023Review
- Cyclophilin B serum levels present variations across the menstrual cycle.Scientific reports · 2023Article
- Article
- Role of SIRT3 in neurological diseases and rehabilitation training.Metabolic brain disease · 2023Review
- NAFLD: Mechanisms, Treatments, and Biomarkers.Biomolecules · 2022Review
- Increase of serum cyclophilin C levels in the follow-up of coronary artery disease: A biomarker and possible clinical predictor.Archivos de cardiologia de Mexico · 2022Article
- Adipose-derived stem cells alleviate liver injury induced by type 1 diabetes mellitus by inhibiting mitochondrial stress and attenuating inflammation.Stem cell research & therapy · 2022Article
- Maternal hypothyroidism during pregnancy alters the function of the retinol-binding protein 4-mediated mitochondrial permeability conversion pore in the kidneys of offspring rats.Clinics (Sao Paulo, Brazil) · 2021Article
- TSH Combined with TSHR Aggravates Diabetic Peripheral Neuropathy by Promoting Oxidative Stress and Apoptosis in Schwann Cells.Oxidative medicine and cellular longevity · 2021Article
- Cyclophilins in Ischemic Heart Disease: Differences Between Acute and Chronic Coronary Artery Disease Patients.Cardiology research · 2020Article
- Thyroid Stimulating Hormone Triggers Hepatic Mitochondrial Stress through Cyclophilin D Acetylation.Oxidative medicine and cellular longevity · 2020Article
- Cyclophilin D participates in the inhibitory effect of high-fat diet on the expression of steroidogenic acute regulatory protein.Journal of cellular and molecular medicine · 2019Article
- High Serum Cyclophilin C levels as a risk factor marker for Coronary Artery Disease.Scientific reports · 2019Article
- Blockade of Cyclophilin D Attenuates Oxidative Stress-Induced Cell Death in Human Dental Pulp Cells.Oxidative medicine and cellular longevity · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsEndothelial cells (ECs) constitute the defensive barrier of vasculature, which maintains the vascular homeostasis. Mitochondrial oxidative stress (mitoOS) in ECs significantly affects the initiation and progression of vascular diseases. The higher serum thyroid stimulating hormone (TSH) level is being recognized as a nonconventional risk factor responsible for the increased risk of cardiovascular diseases in subclinical hypothyroidism (SCH). However, effects and underlying mechanisms of elevated TSH on ECs are still ambiguous. We sought to investigate whether cyclophilin D (CypD), emerging as a crucial mediator in mitoOS, regulates effects of TSH on ECs. METHODS AND
resultsSCH patients with TSH > = 10mIU/L showed a positive correlation between serum TSH and endothelin-1 levels. When TSH levels declined to normal in these subjects after levothyroxine therapy, serum endothelin-1 levels were significantly reduced. Supplemented with exogenous thyroxine to keep normal thyroid hormones, thyroid-specific TSH receptor (TSHR)-knockout mice with injection of exogenous TSH exhibited elevated serum TSH levels, significant endothelial oxidative injuries and disturbed endothelium-dependent vasodilation. However, Tshr
conclusionsThese findings reveal that elevated TSH triggers mitochondrial perturbations in ECs and provide insights that blocking mitochondrial CypD enhances the defensive ability of ECs under TSH exposure.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.