TSHR gene expression and mitochondrial-cardiac interactions as emerging predictors of cardiovascular risk in early thyroid dysfunction.

Authors

Manjusha Kottola, Desigamani Kanniyappan, Damodaran Boopathi, Jeyapal Vidhyadharan, Renjitha Ramachandran, Roshma Retnakaran, Joby Paruthiparayil Jose, Jisha Anjali Madhavan Pillai, Dinesh Roy Divakaran

Published in

Hormone molecular biology and clinical investigation. Oct 01, 2026. Epub Oct 01, 2026.

Abstract

To evaluate biochemical, hormonal, genetic, and mitochondrial alterations associated with cardiovascular risk in SCH, emphasizing the interplay between NT-proBNP, succinate dehydrogenase (SDH) complex activity, and thyroid-stimulating hormone receptor (TSHR) gene expression.
A case-control study was conducted involving SCH patients and age-matched euthyroid controls. Serum thyroid profiles, NT-proBNP, and SDH complex activity were quantified by standard assays, and TSHR gene expression was measured using RT-PCR. Receiver operating characteristic (ROC) analyses assessed diagnostic performance, and multiple linear regression identified independent predictors of TSHR expression.
Compared with controls, SCH cases showed significantly higher TSH and NT-proBNP levels, reduced SDH complex activity, and upregulated TSHR gene expression (p<0.05). ROC analysis demonstrated excellent diagnostic accuracy for NT-proBNP, SDHA, and TSHR expression. After adjustment for confounders, SDH complex activity remained the only independent predictor of TSHR expression, whereas NT-proBNP lost independent significance, suggesting an indirect or interaction-mediated effect.
SDHA serves as a robust independent predictor of cardiovascular risk in SCH, highlighting mitochondrial dysfunction in thyroid receptor regulation. NT-proBNP showed predictive potential but not independent significance, indicating secondary modulation by hormonal or metabolic factors. Larger longitudinal studies are warranted for validation.

PMID:
42814798
Bibliographic data and abstract were imported from PubMed on 01 Oct 2026.

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