Possible Contributions of Nongenomic Actions of Thyroid Hormones to the Vasculopathic Complex of COVID-19 Infection

Paul J. Davis, Hung Yun Lin, Aleck Hercbergs, Kelly A. Keating, Shaker A. Mousa

Research output: Contribution to journalReview articlepeer-review


Background: Integrin αvβ3 is a cell membrane structural protein whose extracellular domain contains a receptor for L-thyroxine (T4). The integrin is expressed in rapidly dividing cells and its internalization is prompted by T4. The protein binds viruses and we have raised the possibility elsewhere that action of free T4 (FT4)—when he latter is increased in the nonthyroidal illness syndrome (NTIS) known to complicate COVID-19 infecction—may enhance cellular uptke of SARS-CoV-2 and its receptor. Objective: Because T4 also acts nongenomically via the integrin to promote platelet aggregation and angiogenesis, we suggest here that T4 may contribute to the coagulopathy and endothelial abnormalities that can develop in COVID-19 infections, particularly when the lung is primary affected. Discussion and Conclusions: Elevated FT4 has been described in the NTIS of COVID-19 patients and may be associated with increased illness severity, but the finding of FT4 elevation is inconsistent in the NTIS literature. Circulating 3,5’,3’-triiodo-L-thyronine (reverse T3, rT3) are frequently elevated in NTIS. Thought to be biologically inactive, rT3in fact stimulates cancer cell proliferation via avb3 and also may increase actin polymerization. We propose here that rT3 in the NTIS complicating systemic COVIF-19 infection may support coagulation and disordered blood vessel formation via actin polymerization.

Original languageEnglish
Pages (from-to)39-44
Number of pages6
JournalEndocrine Research
Issue number1
Publication statusPublished - 2022


  • actin polymerization
  • angiogenesis
  • free T4
  • integrin αvβ3
  • nonthyroidal illness syndrome (NTIS)
  • Reverse T3

ASJC Scopus subject areas

  • Endocrinology


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