ArticleJournal of cardiovascular and thoracic research2026
Exploring cardiovascular risk in subclinical hypothyroidism: The impact of TSHR gene expression and systemic biomarkers.
Article in Journal of cardiovascular and thoracic research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Subclinical hypothyroidism (SCH), defined by elevated thyroid-stimulating hormone (TSH) with normal thyroid hormone levels, affects approximately 3-8% of the population. Growing evidence indicates that thyroid-stimulating hormone receptor (TSHR) expression in cardiovascular tissues, together with systemic inflammation (IL-6) and oxidative stress (3-nitrotyrosine), may contribute to cardiovascular dysfunction in SCH. This study aimed to evaluate the association between TSHR gene expression and systemic biomarkers-hormonal, inflammatory, and oxidative-and to assess their predictive value for cardiovascular risk in SCH patients. Methods: A case-control design was adopted involving 150 SCH subjects and 150 age- and sex-matched healthy controls. Demographic and clinical data were collected using structured interviews. Fasting blood samples were analyzed for TSH (CLIA), IL-6, and 3-nitrotyrosine (ELISA), while TSHR gene expression was quantified using real-time PCR with GAPDH as an internal control. Statistical analyses were performed using Stata version 17.0. Results: Compared with controls, SCH patients showed significantly higher levels of TSH, IL-6, 3-nitrotyrosine, and TSHR gene expression ( Conclusion: SCH is characterized by elevated hormonal, oxidative, and inflammatory markers, with oxidative stress contributing to TSHR upregulation. TSH remains the strongest independent predictor, underscoring the hormonal-oxidative interaction in cardiovascular risk among SCH patients.
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