Abstract
In December 2019, the new acute respiratory syndrome coronavirus 2
(SARS-Cov-2) emerged in Wuhan, China, with an infection of pandemic
proportions. Data from Wuhan showed that mortality from coronavirus
disease 2019 (COVID-19) is strongly associated with cardiovascular
diseases. Similar to SARS-Cov-1, which was responsible for the SARS
epidemic from 2002 to 2004, SARS-Cov-2 also utilizes the host protein
angiotensin II-converting enzyme (ACE2) as a coreceptor to gain
intracellular entry. Hence, upregulation of ACE2 has been proposed as a
potential factor in infectivity and a higher risk of harmful outcomes of
COVID-19. In this context, data obtained from experimental models of
hyperthyroidism have demonstrated increased cardiac ACE2, which can
theoretically facilitate SARS-Cov-2 entry. However, there is currently
no consistent scientific research on how COVID-19 specifically affects
hyperthyroid patients, and more clinical and experimental evidence is
urgently required to clarify this point. In this review, we highlight
important known and unknown features of COVID-19 related to ACE2 and
hyperthyroidism.