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. 2019 Nov 11;105(3):e66–e69. doi: 10.1210/clinem/dgz193

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Published by Oxford University Press on behalf of the Endocrine Society 2019.

This work is written by (a) US Government employee(s) and is in the public domain in the US.

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Figure 1. — Model explaining how cAMP/PKA reduces mROS: TSHR antibodies that do not induce cAMP/PKA are able to induce ROS generation. Neutral mAbs activate ROS, and ROS then induces mitochondrial and ER stress leading to apoptosis of thyrocytes. In contrast, induction of cAMP/PKA (by TSH or stimulating TSHR-Ab) suppresses ROS and prevents apoptosis. (NAC and DPI are inhibitors of ROS and also prevent apoptosis).

Abbreviations: cAMP, adenosine 3',5'-cyclic monophosphate; DPI, diphenylneiodonium; ER, endoplasmic reticulum; mAb, monoclonal antibody; NAC, n-acetyl-l-cysteine; PKA, protein kinase A; mROS, mitochondrial reactive oxygen species; TSH, thyroid-stimulating hormone; TSHR, thyroid-stimulating hormone receptor.