Regulation of nitric oxide production in hypothyroidism.

Zoran M Gluvic, Milan M Obradovic, Emina M Sudar-Milovanovic, Sonja S Zafirovic, Djordje J Radak, Magbubah M Essack, Vladimir B. Bajic, Takashi Gojobori, Esma R Isenovic

Research output: Contribution to journalArticlepeer-review

22 Scopus citations

Abstract

Hypothyroidism is a common endocrine disorder that predominantly occurs in females. It is associated with an increased risk of cardiovascular diseases (CVD), but the molecular mechanism is not known. Disturbance in lipid metabolism, the regulation of oxidative stress, and inflammation characterize the progression of subclinical hypothyroidism. The initiation and progression of endothelial dysfunction also exhibit these changes, which is the initial step in developing CVD. Animal and human studies highlight the critical role of nitric oxide (NO) as a reliable biomarker for cardiovascular risk in subclinical and clinical hypothyroidism. In this review, we summarize the recent literature findings associated with NO production by the thyroid hormones in both physiological and pathophysiological conditions. We also discuss the levothyroxine treatment effect on serum NO levels in hypothyroid patients.
Original languageEnglish (US)
Pages (from-to)109881
JournalBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
Volume124
DOIs
StatePublished - Jan 24 2020

Bibliographical note

KAUST Repository Item: Exported on 2020-10-01
Acknowledged KAUST grant number(s): BAS/1/1606-01-01, FCC/1/1976-17-01
Acknowledgements: This work is part of the collaboration between the Laboratory of Radiobiology and Molecular Genetics, Vinca Institute of Nuclear Sciences, University of Belgrade, Belgrade, Serbia and King Abdullah University of Science and Technology (KAUST), Computational Bioscience Research Center (CBRC), Thuwal, Saudi Arabia. This work has been supported by grants No. 173033 (E.R.I.) and No. 41002 (Dj.R.) from the Ministry of Education, Science and Technological Development, Republic of Serbia and by the KAUST grant OSR#4129 (to E.R.I. and V.B.B.), which also supported E.R.I., M.O., S.Z., and E.S.M. V.B.B. and T.G. has been supported by the KAUST Base Research FundsBAS/1/1606-01-01 and BAS/1/1059-01-01, respectively, while M.E. have been supported by the KAUST Office of Sponsored Research (OSR) grant no. FCC/1/1976-17-01.

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